Podcast
Questions and Answers
What is the primary function of BH3-only proteins in the ER membrane?
What is the primary function of BH3-only proteins in the ER membrane?
What is the consequence when the amount of misfolded proteins is too great to be corrected?
What is the consequence when the amount of misfolded proteins is too great to be corrected?
What is the purpose of the unfolded protein response?
What is the purpose of the unfolded protein response?
What is the term for the process by which the cell dies due to excessive ER stress?
What is the term for the process by which the cell dies due to excessive ER stress?
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What is the location of the sensors that detect misfolded proteins?
What is the location of the sensors that detect misfolded proteins?
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What is the function of the mitochondrial pathway of apoptosis in response to ER stress?
What is the function of the mitochondrial pathway of apoptosis in response to ER stress?
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What is the primary function of molecular oxygen in the process of energy generation?
What is the primary function of molecular oxygen in the process of energy generation?
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What is the consequence of the nutrient deficiency in the mitochondrial pathway?
What is the consequence of the nutrient deficiency in the mitochondrial pathway?
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What is the role of enzymes in the process of energy generation?
What is the role of enzymes in the process of energy generation?
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What is the outcome of the incomplete reduction of molecular oxygen?
What is the outcome of the incomplete reduction of molecular oxygen?
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What is the primary site of reactive oxygen species production?
What is the primary site of reactive oxygen species production?
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What is the consequence of the sequential addition of four electrons to molecular oxygen?
What is the consequence of the sequential addition of four electrons to molecular oxygen?
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What is the role of the mitochondrial pathway in the process of energy generation?
What is the role of the mitochondrial pathway in the process of energy generation?
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What is the underlying mechanism of the reduction of molecular oxygen?
What is the underlying mechanism of the reduction of molecular oxygen?
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What is the Greek origin of the term 'autophagy'?
What is the Greek origin of the term 'autophagy'?
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What is the primary purpose of autophagy in cells?
What is the primary purpose of autophagy in cells?
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What is the characteristic feature of autophagic cells in H&E-stained sections?
What is the characteristic feature of autophagic cells in H&E-stained sections?
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What is the difference between autophagy and necrosis?
What is the difference between autophagy and necrosis?
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What is the fate of cellular components in autophagic cells?
What is the fate of cellular components in autophagic cells?
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What is the consequence of autophagy on cellular ATP production?
What is the consequence of autophagy on cellular ATP production?
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What is the role of lysosomes in autophagy?
What is the role of lysosomes in autophagy?
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What is the morphological appearance of autophagic cells?
What is the morphological appearance of autophagic cells?
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What is the primary consequence of excessive production or inadequate removal of reactive oxygen species (ROS) in cells?
What is the primary consequence of excessive production or inadequate removal of reactive oxygen species (ROS) in cells?
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What is the role of superoxide dismutase (SOD) in cells?
What is the role of superoxide dismutase (SOD) in cells?
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Which of the following is a consequence of reactive oxygen species (ROS) accumulation in cells?
Which of the following is a consequence of reactive oxygen species (ROS) accumulation in cells?
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What is the relationship between reactive oxygen species (ROS) and cellular injury?
What is the relationship between reactive oxygen species (ROS) and cellular injury?
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Which enzymatic system is responsible for removing reactive oxygen species (ROS) in cells?
Which enzymatic system is responsible for removing reactive oxygen species (ROS) in cells?
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What is the consequence of inadequate removal of reactive oxygen species (ROS) in cells?
What is the consequence of inadequate removal of reactive oxygen species (ROS) in cells?
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Reactive oxygen species (ROS) can damage which of the following cellular components?
Reactive oxygen species (ROS) can damage which of the following cellular components?
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What is the role of reactive oxygen species (ROS) in toxin-mediated cell injury?
What is the role of reactive oxygen species (ROS) in toxin-mediated cell injury?
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What is the primary mechanism underlying the development of hyperplasia?
What is the primary mechanism underlying the development of hyperplasia?
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Which of the following is a consequence of hyperplasia in the breast tissue?
Which of the following is a consequence of hyperplasia in the breast tissue?
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What is the role of growth factors in hyperplasia?
What is the role of growth factors in hyperplasia?
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Which of the following diseases is associated with hyperplasia?
Which of the following diseases is associated with hyperplasia?
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What is the consequence of surviving cells after death or removal of some cells in an organ?
What is the consequence of surviving cells after death or removal of some cells in an organ?
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What is the role of hormones in hyperplasia?
What is the role of hormones in hyperplasia?
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Which of the following is a characteristic of hyperplasia?
Which of the following is a characteristic of hyperplasia?
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What is the consequence of increased growth factor production in hyperplasia?
What is the consequence of increased growth factor production in hyperplasia?
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The mitochondrial pathway and death receptor pathway of apoptosis share the same induction mechanism.
The mitochondrial pathway and death receptor pathway of apoptosis share the same induction mechanism.
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BH3-only proteins activate caspases directly.
BH3-only proteins activate caspases directly.
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The end result of both apoptosis pathways is the inhibition of cell growth.
The end result of both apoptosis pathways is the inhibition of cell growth.
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BCL-2 proteins maintain mitochondrial permeability.
BCL-2 proteins maintain mitochondrial permeability.
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Caspases are involved in the regulation of cell survival.
Caspases are involved in the regulation of cell survival.
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The death receptor pathway involves the activation of adaptor proteins.
The death receptor pathway involves the activation of adaptor proteins.
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Mitochondrial permeability is increased in the death receptor pathway.
Mitochondrial permeability is increased in the death receptor pathway.
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Cytochrome c is released from the mitochondria in the death receptor pathway.
Cytochrome c is released from the mitochondria in the death receptor pathway.
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Hypoxia and Ischemia lead to increased production of ATP in mitochondria.
Hypoxia and Ischemia lead to increased production of ATP in mitochondria.
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In the absence of oxygen, energy-dependent cellular systems fail due to increased ATP production.
In the absence of oxygen, energy-dependent cellular systems fail due to increased ATP production.
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Cytochrome P450 generates reactive oxygen species during phagocytosis.
Cytochrome P450 generates reactive oxygen species during phagocytosis.
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Precision medicine uses gene expression to predict how a microbe responds to oxidative stress.
Precision medicine uses gene expression to predict how a microbe responds to oxidative stress.
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The sequential addition of four electrons to molecular oxygen leads to the formation of water.
The sequential addition of four electrons to molecular oxygen leads to the formation of water.
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Reactive oxygen species are produced in the mitochondrial pathway of energy generation.
Reactive oxygen species are produced in the mitochondrial pathway of energy generation.
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The primary function of cytochrome P450 is to metabolize endogenous compounds.
The primary function of cytochrome P450 is to metabolize endogenous compounds.
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Phagocytosis is a process that occurs in the endoplasmic reticulum.
Phagocytosis is a process that occurs in the endoplasmic reticulum.
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Autophagy is a process of cellular injury that leads to cell death.
Autophagy is a process of cellular injury that leads to cell death.
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The primary consequence of inadequate removal of reactive oxygen species is cellular hypertrophy.
The primary consequence of inadequate removal of reactive oxygen species is cellular hypertrophy.
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Cytochrome P450 is involved in the reduction of molecular oxygen to form water.
Cytochrome P450 is involved in the reduction of molecular oxygen to form water.
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Reactive oxygen species can damage cellular components such as proteins, lipids, and DNA.
Reactive oxygen species can damage cellular components such as proteins, lipids, and DNA.
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Superoxide dismutase is an enzyme that produces reactive oxygen species.
Superoxide dismutase is an enzyme that produces reactive oxygen species.
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The goal of precision medicine is to use gene expression to predict the efficacy of antibiotics.
The goal of precision medicine is to use gene expression to predict the efficacy of antibiotics.
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Hyperplasia is a process of cellular differentiation that leads to tissue development.
Hyperplasia is a process of cellular differentiation that leads to tissue development.
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Phagocytosis is a process that occurs in the mitochondria.
Phagocytosis is a process that occurs in the mitochondria.
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Deprivation of glucose and oxygen can increase the burden of environmental and microbial toxins.
Deprivation of glucose and oxygen can increase the burden of environmental and microbial toxins.
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Many environmental and microbial toxins can directly damage cellular components.
Many environmental and microbial toxins can directly damage cellular components.
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Cytochrome P450 is responsible for converting toxins into reactive metabolites in liver cells.
Cytochrome P450 is responsible for converting toxins into reactive metabolites in liver cells.
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Diseases caused by misfolded proteins are not associated with environmental toxins.
Diseases caused by misfolded proteins are not associated with environmental toxins.
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Reactive oxygen species can be produced through the sequential addition of four electrons to molecular oxygen.
Reactive oxygen species can be produced through the sequential addition of four electrons to molecular oxygen.
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Mitochondrial dysfunction is not a consequence of environmental toxin exposure.
Mitochondrial dysfunction is not a consequence of environmental toxin exposure.
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ER stress can induce apoptosis through the activation of p53.
ER stress can induce apoptosis through the activation of p53.
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Autophagy is a process of programmed cell death.
Autophagy is a process of programmed cell death.
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Reactive oxygen species (ROS) are primarily produced in the mitochondria.
Reactive oxygen species (ROS) are primarily produced in the mitochondria.
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The unfolded protein response can lead to cell death through the activation of caspases.
The unfolded protein response can lead to cell death through the activation of caspases.
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Hyperplasia is a process of programmed cell death.
Hyperplasia is a process of programmed cell death.
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BH3-only proteins are involved in the regulation of mitochondrial permeability.
BH3-only proteins are involved in the regulation of mitochondrial permeability.
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The mitochondrial pathway of apoptosis is inhibited by BCL-2 proteins.
The mitochondrial pathway of apoptosis is inhibited by BCL-2 proteins.
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DNA damage can be repaired through the activation of p53.
DNA damage can be repaired through the activation of p53.
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What is the primary consequence of cellular injury resulting from abnormalities in one or more essential cellular components?
What is the primary consequence of cellular injury resulting from abnormalities in one or more essential cellular components?
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Which cellular components are primarily affected by cellular injury?
Which cellular components are primarily affected by cellular injury?
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What is the role of myeloperoxidase in cellular injury?
What is the role of myeloperoxidase in cellular injury?
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What is the consequence of excessive production or inadequate removal of reactive oxygen species (ROS) in cells?
What is the consequence of excessive production or inadequate removal of reactive oxygen species (ROS) in cells?
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Which enzymatic system is responsible for removing reactive oxygen species (ROS) in cells?
Which enzymatic system is responsible for removing reactive oxygen species (ROS) in cells?
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What is the primary mechanism underlying the development of hyperplasia?
What is the primary mechanism underlying the development of hyperplasia?
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What is the primary source of reactive oxygen species in cells?
What is the primary source of reactive oxygen species in cells?
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What is the consequence of surviving cells after death or removal of some cells in an organ?
What is the consequence of surviving cells after death or removal of some cells in an organ?
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What is the role of superoxide dismutase in cells?
What is the role of superoxide dismutase in cells?
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What is the role of reactive oxygen species (ROS) in toxin-mediated cell injury?
What is the role of reactive oxygen species (ROS) in toxin-mediated cell injury?
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What is the consequence of excessive production or inadequate removal of reactive oxygen species?
What is the consequence of excessive production or inadequate removal of reactive oxygen species?
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What is the outcome of the sequential addition of four electrons to molecular oxygen?
What is the outcome of the sequential addition of four electrons to molecular oxygen?
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What is the primary mechanism underlying the development of cellular injury?
What is the primary mechanism underlying the development of cellular injury?
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What is the role of enzymes in the removal of reactive oxygen species?
What is the role of enzymes in the removal of reactive oxygen species?
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What is the relationship between cellular ATP production and reactive oxygen species?
What is the relationship between cellular ATP production and reactive oxygen species?
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What is the consequence of inadequate removal of reactive oxygen species in cells?
What is the consequence of inadequate removal of reactive oxygen species in cells?
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What is the consequence of the accumulation of misfolded proteins in the ER?
What is the consequence of the accumulation of misfolded proteins in the ER?
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What is the role of molecular chaperones in the ER?
What is the role of molecular chaperones in the ER?
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What is the consequence of ER stress on cellular aging?
What is the consequence of ER stress on cellular aging?
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How do BH3-only proteins contribute to the unfolded protein response?
How do BH3-only proteins contribute to the unfolded protein response?
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What is the consequence of the inhibition of the unfolded protein response?
What is the consequence of the inhibition of the unfolded protein response?
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What is the role of the mitochondrial pathway in the response to ER stress?
What is the role of the mitochondrial pathway in the response to ER stress?
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How does the unfolded protein response impact cellular metabolism?
How does the unfolded protein response impact cellular metabolism?
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What is the consequence of the activation of the unfolded protein response on cellular longevity?
What is the consequence of the activation of the unfolded protein response on cellular longevity?
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What is the consequence of patrologic adapters and oncogenic transformation in cells?
What is the consequence of patrologic adapters and oncogenic transformation in cells?
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What happens to cellular components in autophagic cells?
What happens to cellular components in autophagic cells?
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What is the outcome of inadequate removal of reactive oxygen species in cells?
What is the outcome of inadequate removal of reactive oxygen species in cells?
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What is the role of hormones in hyperplasia?
What is the role of hormones in hyperplasia?
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What is the consequence of atrophy in cells?
What is the consequence of atrophy in cells?
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What is the result of mechanical stress on cells?
What is the result of mechanical stress on cells?
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What is the outcome of patological adaptations in cells?
What is the outcome of patological adaptations in cells?
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What is the consequence of excessive production of reactive oxygen species in cells?
What is the consequence of excessive production of reactive oxygen species in cells?
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What is the role of ceramide in the mitochondrial pathway of apoptosis?
What is the role of ceramide in the mitochondrial pathway of apoptosis?
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What is the consequence of excessive ER stress on cellular membranes?
What is the consequence of excessive ER stress on cellular membranes?
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How do BH3-only proteins contribute to the regulation of mitochondrial permeability?
How do BH3-only proteins contribute to the regulation of mitochondrial permeability?
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What is the role of reactive oxygen species (ROS) in cellular injury?
What is the role of reactive oxygen species (ROS) in cellular injury?
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How do growth factors contribute to the development of hyperplasia?
How do growth factors contribute to the development of hyperplasia?
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What is the consequence of inadequate removal of reactive oxygen species (ROS) in cells?
What is the consequence of inadequate removal of reactive oxygen species (ROS) in cells?
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How do cellular membranes respond to ER stress?
How do cellular membranes respond to ER stress?
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What is the role of autophagy in cellular homeostasis?
What is the role of autophagy in cellular homeostasis?
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The ______ necrosis factor receptor family is found on many cells.
The ______ necrosis factor receptor family is found on many cells.
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The ______ reticulum is involved in the process of cell death.
The ______ reticulum is involved in the process of cell death.
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Type I ______ receptor is a death receptor that mediates apoptosis.
Type I ______ receptor is a death receptor that mediates apoptosis.
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FAS is a ______ protein that is expressed on many cells.
FAS is a ______ protein that is expressed on many cells.
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The ______ domain is a protein domain that is involved in cell death.
The ______ domain is a protein domain that is involved in cell death.
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FAS is a ______ that is involved in the process of apoptosis.
FAS is a ______ that is involved in the process of apoptosis.
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The ______ receptor is a death receptor that is involved in apoptosis.
The ______ receptor is a death receptor that is involved in apoptosis.
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The ______ pathway is a pathway of cell death that is mediated by death receptors.
The ______ pathway is a pathway of cell death that is mediated by death receptors.
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ROS are produced normally in small amounts in a __________ during the reduction-oxidation reactions.
ROS are produced normally in small amounts in a __________ during the reduction-oxidation reactions.
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The process of reduction-oxidation reactions occurs during __________ response and energy generation.
The process of reduction-oxidation reactions occurs during __________ response and energy generation.
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In the process of energy generation, molecular oxygen is __________ to generate water.
In the process of energy generation, molecular oxygen is __________ to generate water.
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The addition of four electrons to molecular oxygen results in the formation of __________.
The addition of four electrons to molecular oxygen results in the formation of __________.
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The incomplete reduction of molecular oxygen results in the formation of __________.
The incomplete reduction of molecular oxygen results in the formation of __________.
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The primary site of __________ production is the mitochondria.
The primary site of __________ production is the mitochondria.
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The nutrient deficiency can trigger the __________ pathway of apoptosis.
The nutrient deficiency can trigger the __________ pathway of apoptosis.
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The mitochondrial pathway of apoptosis can result in the death of a __________.
The mitochondrial pathway of apoptosis can result in the death of a __________.
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Cell injury results from abnormalities in one or more essential ______ components.
Cell injury results from abnormalities in one or more essential ______ components.
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The major component of the cell affected by oxidative stress is the ______.
The major component of the cell affected by oxidative stress is the ______.
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The enzyme responsible for converting a reactive compound into a reactive oxygen species is ______.
The enzyme responsible for converting a reactive compound into a reactive oxygen species is ______.
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The consequence of impaired function of essential ______ components is inflammation.
The consequence of impaired function of essential ______ components is inflammation.
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The presence of ______ in neutrophil granules is one reason for the consequences of oxidative stress.
The presence of ______ in neutrophil granules is one reason for the consequences of oxidative stress.
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In the absence of oxygen, _______________ glycolysis increases, resulting in an increase in the production of lactic acid.
In the absence of oxygen, _______________ glycolysis increases, resulting in an increase in the production of lactic acid.
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The damage caused by reactive oxygen species can lead to ______ of normal tissues.
The damage caused by reactive oxygen species can lead to ______ of normal tissues.
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_________________ phosphorylation is a process that generates ATP in the presence of oxygen.
_________________ phosphorylation is a process that generates ATP in the presence of oxygen.
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The process of energy generation in the mitochondria involves the use of ______ oxygen.
The process of energy generation in the mitochondria involves the use of ______ oxygen.
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Rough endoplasmic reticulum (RER) releases _______________ that detach from the ER, leading to reduced protein synthesis.
Rough endoplasmic reticulum (RER) releases _______________ that detach from the ER, leading to reduced protein synthesis.
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The absence of oxygen results in a decrease in the activity of many _______________ enzymes.
The absence of oxygen results in a decrease in the activity of many _______________ enzymes.
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The incomplete reduction of ______ oxygen can lead to the formation of reactive oxygen species.
The incomplete reduction of ______ oxygen can lead to the formation of reactive oxygen species.
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The decrease in pH and the increase in lactic acid production are a consequence of the increased _______________ glycolysis.
The decrease in pH and the increase in lactic acid production are a consequence of the increased _______________ glycolysis.
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In the absence of oxygen, the energy-dependent cellular systems fail due to the decreased production of _______________.
In the absence of oxygen, the energy-dependent cellular systems fail due to the decreased production of _______________.
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The process of energy generation in the mitochondria is dependent on the presence of _______________ oxygen.
The process of energy generation in the mitochondria is dependent on the presence of _______________ oxygen.
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The reduced activity of _______________ enzymes leads to a decrease in ATP production in the mitochondria.
The reduced activity of _______________ enzymes leads to a decrease in ATP production in the mitochondria.
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The functional and morphologic consequences of hypoxia and ischemia may release _______________ that cause more damage.
The functional and morphologic consequences of hypoxia and ischemia may release _______________ that cause more damage.
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The production of ROS can cause _______________ peroxidation and membrane damage.
The production of ROS can cause _______________ peroxidation and membrane damage.
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Reperfusion can lead to the production of _______________ radicals.
Reperfusion can lead to the production of _______________ radicals.
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The conversion of H2O2 to H2O is done by _______________ peroxidase.
The conversion of H2O2 to H2O is done by _______________ peroxidase.
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The removal of free radicals is done by _______________ dismutase.
The removal of free radicals is done by _______________ dismutase.
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The primary site of reactive oxygen species production is the _______________.
The primary site of reactive oxygen species production is the _______________.
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The incomplete reduction of molecular oxygen can lead to the formation of _______________ oxygen species.
The incomplete reduction of molecular oxygen can lead to the formation of _______________ oxygen species.
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The primary consequence of excessive production or inadequate removal of ROS is _______________ cellular injury.
The primary consequence of excessive production or inadequate removal of ROS is _______________ cellular injury.
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The role of superoxide dismutase is to remove _______________ oxygen species from cells.
The role of superoxide dismutase is to remove _______________ oxygen species from cells.
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Reactive oxygen species can damage _______________ components in cells.
Reactive oxygen species can damage _______________ components in cells.
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Match the following reactive oxygen species with their corresponding effects:
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Study Notes
Autophagy
- Autophagy is a form of "self-eating" (Greek, phaga = to eat) where cells recycle their own organelles to provide energy for survival.
- Autophagy is different from necrosis, and it is a type of programmed cell death.
Morphological Appearance
- In H&E-stained sections, the nucleus appears mature to provide energy for survival.
- During autophagy, organelles condense, and the cells are shrunken, appearing in vacuoles.
ROS and Cell Injury
- ROS (Reactive Oxygen Species) are produced normally in small amounts during reduction-oxidation (redox) reactions in mitochondria.
- ROS can trigger apoptosis by the mitochondrial pathway if not corrected.
- The production of ROS is increased by many injurious stimuli, and excessive production or inadequate removal leads to accumulation of free radicals in cells, causing cell injury.
Unfolded Protein Response and Endoplasmic Reticulum (ER) Stress
- The presence of misfolded proteins in the ER is detected by sensors in the ER membrane, triggering an adaptive unfolded protein response.
- If the amount of misfolded proteins is too great to be corrected, the mitochondrial pathway of apoptosis is induced, and the irreparably damaged cell dies.
Hyperplasia
- Hyperplasia can be physiological or pathological and is characterized by an increased growth rate of cells.
- Growth factors are produced by a variety of cell types, and some are produced by hormones.
- Hyperplasia can be induced by various factors, such as insulin-like growth factor-1 (IGF-1), leading to increased DNA replication and cell proliferation.
Mechanisms of Apoptosis
- There are two pathways of apoptosis: the mitochondrial pathway and the death receptor pathway
- Both pathways culminate in the activation of caspases, leading to cell death and fragmentation
- In the mitochondrial pathway, BH3-only proteins sense a lack of survival signals or DNA damage and activate effector molecules, increasing mitochondrial permeability
- This leads to the release of cytochrome c into the cytosol, activating caspases
- In the death receptor pathway, signals from plasma membrane receptors lead to the assembly of adaptor proteins into a "death-inducing signaling complex", which activates caspases
ROS Production and Its Effects
- ROS (Reactive Oxygen Species) are produced during phagocytosis in leukocytes, mainly neutrophils and macrophages, to destroy ingested microbes and other substances
- ROS can affect many chemicals and enzymes, leading to oxidative damage and oxidative stress
- Increased generation of ROS in coronary artery disease, a major cause of myocardial infarction, can lead to severe damage
Hypoxia and Ischemia
- Hypoxia leads to reduced generation of ATP and failure of energy-dependent cellular systems
- Oxygen deficiency can lead to increased ROS production, damaging cellular components and leading to disease
Cellular Damage and Apoptosis
- Many environmental and microbial toxins can damage cellular components directly or after conversion to reactive metabolites
- Damaged DNA activates p53, arresting cells in the G1 phase to allow for repair
- If DNA damage is extensive, p53 triggers apoptosis through the mitochondrial pathway
Cell Injury and Death
- Cell injury results from abnormalities in one or more essential cellular components, mainly mitochondria, membranes, and the nucleus.
- The consequences of impairment of each of these cellular components are distinct but overlapping.
- Mitochondria, whose function is to generate energy, can release factors that trigger cell death.
- Mitochondrial dysfunction can lead to the release of cytochrome c, which activates the caspase cascade, a process that ultimately leads to cell death.
- Cell membranes are composed of lipids and proteins, and their disruption can lead to cell injury.
- The nucleus, which contains the cell's genetic material, is essential for cellular function and survival.
Oxidative Stress and Cell Injury
- Oxidative stress, which occurs when the amount of oxygen in the cell is partially reduced, can generate reactive oxygen species (ROS) such as superoxide and hydrogen peroxide.
- ROS can damage cellular components, including proteins, lipids, and DNA, leading to cell injury.
- Superoxide dismutase is an enzyme that converts superoxide into hydrogen peroxide, which is then broken down into water and oxygen.
- Oxidative stress can trigger cell death through the activation of pro-apoptotic pathways.
Proteins and Cell Injury
- Impaired protein function or misfolded proteins can accumulate in the endoplasmic reticulum (ER), leading to ER stress.
- ER stress can trigger the unfolded protein response (UPR), which is a pro-survival response that aims to restore protein homeostasis.
- If the UPR is unsuccessful, it can trigger cell death through the activation of pro-apoptotic pathways.
- Misfolded proteins can also accumulate in the cytosol, leading to the activation of proteolytic pathways that degrade the proteins.
Aging and Cell Injury
- Cellular aging is a process that contributes to the development of many degenerative, metabolic, and neoplastic disorders.
- The process of aging is focused on the cosmetic and physical consequences of aging, but the real danger lies in the development of cellular aging.
- Cellular aging is characterized by the accumulation of misfolded proteins, oxidative stress, and mitochondrial dysfunction.
- These changes can lead to the activation of pro-apoptotic pathways and cell death.
Atrophy
- Atrophy is a decrease in the number of cells and, therefore, may cause a loss of functional capacity.
- Atrophy is caused by the reduction of cellular components, such as proteins, and can lead to cell death.
- Physiological and pathological adaptations can occur in response to atrophy, which can lead to changes in cellular structure and function.
Cell Injury and Cell Death
- Cell injury can result from abnormalities in one or more essential cellular components, mainly mitochondria, membranes, and the nucleus.
- Consequences of cell injury can be disparate, but overlapping, and can lead to cell death.
TNF Receptors and Cell Death
- TNF receptors are found on many cells and have a "death domain" that mediates interaction with other proteins.
- The death domain is a conserved region in the intracellular part of the receptor that mediates the activation of downstream signaling pathways.
- Activation of TNF receptors can trigger apoptosis and necrosis.
FAS Receptors and Cell Death
- FAS receptors are a type of death receptor that induces apoptosis when activated by FAS ligand (FASL).
- FAS receptors are expressed on many cells, including activated T lymphocytes, and are involved in the regulation of immune responses.
- Activation of FAS receptors can trigger apoptosis and necrosis.
ROS and Cell Death
- ROS (reactive oxygen species) are produced normally in small amounts during cellular metabolism, but can accumulate in response to cell injury or stress.
- Excessive production of ROS can lead to oxidative stress, which can cause cell damage and death.
- ROS can trigger apoptosis and necrosis by activating signaling pathways that promote cell death.
Mitochondrial Dysfunction and Cell Death
- Mitochondrial dysfunction can lead to cell death by impairing energy production and promoting the release of pro-apoptotic factors.
- Mitochondrial dysfunction can be caused by various factors, including oxidative stress, DNA damage, and mutations in mitochondrial DNA.
Anaerobic Glycolysis and Cell Death
- Anaerobic glycolysis is a metabolic pathway that occurs in the absence of oxygen, resulting in the production of ATP and lactic acid.
- Increased anaerobic glycolysis can lead to acidification of the cell, decreased pH, and reduced activity of cellular enzymes.
- Anaerobic glycolysis can contribute to cell death by promoting acidosis and reducing cellular energy production.
Endoplasmic Reticulum Stress and Cell Death
- Endoplasmic reticulum (ER) stress occurs when the ER is unable to properly fold and process proteins.
- ER stress can trigger apoptosis and necrosis by activating signaling pathways that promote cell death.
- ER stress can be caused by various factors, including oxidative stress, DNA damage, and mutations in genes involved in protein synthesis.
Pathologic Effects of Cell Injury
- Cell injury can lead to various pathologic effects, including inflammation, immune responses, and tissue damage.
- The consequences of cell injury can depend on the type and severity of the injury, as well as the specific cellular components involved.
Mechanisms of Cell Injury and Death
- Cell injury occurs when oxygen is partially reduced, generating superoxides, hydrogen peroxide, and hydroxyl radicals.
- Superoxides are converted to hydrogen peroxide spontaneously and by the action of the enzyme superoxide dismutase.
- Mitochondrial dysfunction leads to anaerobic glycolysis, increasing lactic acid production, decreasing intracellular pH, and reducing cellular activities.
Oxidative Phosphorylation
- Oxidative phosphorylation is impaired, reducing ATP generation in the absence of oxygen.
- Decreased intracellular pH and reduced activity of many intracellular enzymes occur as a result.
Ribosomes and Protein Synthesis
- Ribosomes detach from the Endoplasmic Reticulum (ER), leading to reduced protein synthesis.
- Telomeres shorten, associated with decreased capacity to correct mistakes, leading to accumulating errors.
ER Stress and Unfolded Protein Response
- Mild ER stress leads to an adaptive response, increasing chaperone synthesis and protein degradation.
- Severe ER stress leads to a terminal unfolded protein response, activating BH3 proteins and caspases, ultimately resulting in apoptosis.
Cell Death
- Atrophy is a decrease in cell number, potentially causing an escape from injury but at the expense of normal function.
- Physiological and organ shrinkage can occur as a result.
Cell Injury and Adaptation
- Persistent pathological mediators, such as hormone-induced enlargement of breast tissue and hyperplasia, can lead to cell injury.
- Mechanical stress, such as bone and muscle development, can also cause cell injury.
- Pathological adaptations are responses to mutations and oncogenic transformations, allowing cells to modify their structure and function.
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This quiz covers the concept of hyperplasia, including its types, causes, and effects on cell growth and division. It also explores the role of hormones in regulating cell growth and DNA replication.