Vitamins Overview Quiz

Organic nutrients required in small amounts for various biochemical functions that the body cannot produce; must be obtained from diet.

Vitamins that are hydrophobic (water-repelling) thus require fat for efficient absorption in the body.

Deficiency in vitamin A, resulting in night blindness and a condition where the cornea becomes dry and hard.

A softening of bones in adults, often caused by vitamin D deficiency.

A substance that protects the cells of the body from damage by free radicals.

The process of converting carotenoids into vitamin A.

The visual pigment found in the rod cells of the retina, composed of 11-cis retinal and the protein opsin.

The process of retinaldehyde being converted back to 11-cis retinal for rhodopsin regeneration after exposure to light.

Vitamin D deficiency in children, leading to weak and deformed bones due to poor calcium absorption.

The active form of vitamin D, produced by the kidneys, which directly regulates calcium levels in the body.

The process of converting inactive forms of vitamin D (D2 and D3) into the active form, calcitriol.

A deficiency in vitamin D that can lead to rickets in children and osteomalacia in adults.

Vitamin D's main role is to control calcium levels in the blood.

Calcitriol (active vitamin D) increases calcium absorption in the intestines, helping the body obtain more calcium.

Calcitriol reduces calcium loss in the urine by stimulating reabsorption in the kidneys.

Thiamin diphosphate, a coenzyme, plays a key role in the oxidation of carbohydrates, particularly in the conversion of pyruvate.

Thiamin deficiency leads to a chronic peripheral neuropathy, affecting nerve function, especially in the legs and arms, often accompanied by heart failure and edema.

Loss of appetite, general fatigue, digestive problems, and numbness in limbs are common symptoms of thiamin deficiency.

Wernicke's encephalopathy is a neurological disorder associated with thiamin deficiency, mainly caused by chronic alcohol misuse, leading to confusion, vision problems, and memory impairment.

Pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and branched-chain keto-acid dehydrogenase are all multi-enzyme complexes that rely on thiamin diphosphate for their function.

A deficiency of thiamin can lead to two distinct but often interconnected conditions: Wernicke's disease and Korsakoff syndrome.

Dry beriberi primarily affects the peripheral nerves, causing muscle atrophy and loss of reflexes, while wet beriberi is more severe, resulting in edema due to heart failure.

Thiamin deficiency is particularly linked to alcohol abuse and chronic misuse, as alcohol interferes with the absorption and utilization of this vital vitamin.

The conversion of methylene-tetrahydrofolate to methyl-tetrahydrofolate is an irreversible process, and methyl-tetrahydrofolate is the primary source of tetrahydrofolate for tissues. This makes methionine synthase crucial, bridging folate and vitamin B12 functions.

In vitamin B12 deficiency, methionine synthase is impaired, leading to the accumulation of methyltetrahydrofolate, which traps folate in an unusable form.

Vitamin B12 deficiency results in a functional deficiency of folate, even if adequate dietary folate is present because the body cannot utilize the trapped folate.

Cells that divide rapidly require thymidine for DNA synthesis. Both folic acid deficiency and vitamin B12 deficiency ( leading to functional folic acid deficiency) disrupt this process.

Megaloblastic anemia is a condition characterized by the production of abnormally large red blood cells, caused by impaired DNA synthesis due to folate or vitamin B12 deficiency. This affects the bone marrow, the site of red blood cell production.

Vitamin C is a vitamin for humans and certain animals, but other animals can synthesize it. The lack of gulonolactone oxidase, an enzyme involved in vitamin C synthesis, leads to its deficiency in these animals.

Vitamin C plays specific roles in certain hydroxylases like dopamine -hydroxylase, which is involved in catecholamine synthesis. Ascorbic acid reduces Cu2+ to Cu+ in this process.

In addition to its enzymatic roles, vitamin C functions as a reducing agent and an oxygen radical quencher, protecting against oxidative damage.

The molecule Coenzyme A (CoA) is formed by combining pantothenic acid (vitamin B5) with cysteine. This combination provides the functional component (prosthetic group) containing a sulfur atom (-SH) that is essential for CoA's role in various metabolic processes.

Coenzyme A (CoA) plays a crucial role in the citric acid cycle (Krebs cycle), fatty acid breakdown (oxidation), transferring acetyl groups (acetylations), and cholesterol synthesis.

Acyl Carrier Protein (ACP) is a crucial component in the synthesis of fatty acids, helping to transport fatty acid building blocks during the process.

Although synthesized by microorganisms, vitamin B12 (cobalamin) is mainly found in foods of animal origin. This means people who follow a strict vegetarian diet (vegans) are at risk of developing vitamin B12 deficiency.

Pernicious anemia is a type of anemia caused by vitamin B12 deficiency, which ultimately impairs the use of folate (vitamin B9) in the body. This disruption in folate metabolism disrupts red blood cell production, leading to the release of abnormally large and immature red blood cells (megaloblasts) into the bloodstream.

The active form of folic acid (pteroyl glutamate) is tetrahydrofolate. Tetrahydrofolate is involved in various metabolic reactions, including transferring one-carbon units (methyl, formyl, etc.). These one-carbon units are crucial for synthesis of DNA, amino acids, and other essential compounds.

S-adenosylmethionine (SAM) is a crucial molecule involved in methylation reactions. It donates a methyl group to homocysteine, regenerating methionine. The regeneration of methionine is catalyzed by the enzyme methionine synthase, which requires vitamin B12 as a cofactor.

Methylmalonyl CoA mutase, leucine aminomutase, and methionine synthase are all enzymes that require vitamin B12 for their activity. These enzymes are essential for specific metabolic processes, including fatty acid metabolism and protein synthesis.

Thiamin diphosphate (TPP) is a coenzyme essential for pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA. Thiamine deficiency leads to impaired conversion, causing a buildup of pyruvate and lactate. This can lead to life-threatening lactic acidosis, especially for people with a high carbohydrate diet.

Riboflavin is a precursor to FMN and FAD, important coenzymes for energy production. FMN is formed from riboflavin via phosphorylation, while FAD is further synthesized with an AMP moiety added to FMN.

Riboflavin deficiency can lead to impaired energy production due to reduced activity of enzymes, like dihydrolipoyl dehydrogenase and succinate dehydrogenase, which rely on riboflavin derived coenzymes. However, this deficiency is typically not fatal due to efficient conservation and reutilization of tissue riboflavin.

The coenzyme NAD, derived from niacin, is essential for oxidation-reduction reactions and plays a role in DNA repair by providing ADP-ribose for protein and polyADP-ribosylation.

Pellagra is a disease caused by niacin deficiency. It is characterized by dermatitis (skin problems), dementia, and diarrhea. Untreated pellagra can be fatal. The deficiency of riboflavin or vitamin B6 can exacerbate pellagra by impairing tryptophan conversion to nicotinamide.

Niacin is a vital nutrient that can be synthesized from tryptophan, an essential amino acid. The active forms of niacin are nicotinic acid and nicotinamide, which are essential components of the coenzymes NAD and NADP.

Niacin is crucial for the function of NAD and NADP, essential coenzymes involved in redox reactions. These coenzymes play a critical role in numerous metabolic pathways, including energy production, DNA repair, and cell signaling.

Riboflavin deficiency is common in developing nations where access to milk and dairy products, the main dietary sources, is limited. However, the condition is usually not fatal due to efficient conservation and reutilization of tissue riboflavin.