Biochemistry chapter
SubjectsBiochemistry
BIOCHEMISTRY

Micronutrients: Vitamins & Minerals

136 practice questions · 55 study notes
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Questions

QUESTION 1
Which vitamin K compound is the normal dietary source found in green vegetables?
QUESTION 2
Which cell membrane property does vitamin E help maintain?
QUESTION 3
How does pyridoxal phosphate terminate steroid hormone action?
QUESTION 4
During dopamine β-hydroxylase activity, what is the specific role of ascorbate?
QUESTION 5
Under which condition is muscle-associated pyridoxal phosphate released to support increased gluconeogenesis from amino acids?
QUESTION 6
During vitamin B12 absorption, what happens to cobalophilin in the duodenum?
QUESTION 7
The most widely used functional assessment of vitamin B6 status measures activation of which enzymes after adding pyridoxal phosphate in vitro?
QUESTION 8
Moderate vitamin B6 deficiency causes abnormalities in the metabolism of which pair of amino acids?
QUESTION 9
Which vitamin E vitamer has the greatest biological potency?
QUESTION 10
Trimethyllysine hydroxylase and γ-butyrobetaine hydroxylase are required for synthesis of which compound?
QUESTION 11
Vitamin B12 deficiency reduces methylmalonyl-CoA mutase activity. Increased urinary excretion of which compound provides a means of assessing this deficiency?
QUESTION 12
In iron-containing, ascorbate-requiring hydroxylases, substrate hydroxylation is linked to which reaction?
QUESTION 13
Which vitamin K compounds are synthesized by intestinal bacteria and have side chains of differing lengths?
QUESTION 14
From which intestinal region is the intrinsic factor–vitamin B12 complex absorbed?
QUESTION 15
A patient takes 2–7 g of pyridoxine daily and develops neurological toxicity. Which manifestation is specifically associated with this exposure?
QUESTION 16
Impairment of methionine synthase in vitamin B12 deficiency traps folate in which form?
QUESTION 17
Which product can be formed by oxidation of the apo-carotenals generated through asymmetric cleavage of β-carotene?
QUESTION 18
Which feature of thiamin diphosphate enables its initial addition to a substrate carbonyl group during oxidative decarboxylation?
QUESTION 19
Which enzyme of the pentose phosphate pathway uses thiamin diphosphate as its coenzyme?
QUESTION 20
Why may a relatively large proportion of ingested β-carotene appear unchanged in the circulation?
QUESTION 21
Niacin performs its metabolic function as which component of coenzymes involved in oxidation/reduction reactions?
QUESTION 22
Approximately how much tryptophan is equivalent to 1 mg of dietary niacin?
QUESTION 23
Which enzyme cleaves β-carotene and other provitamin A carotenoids in the intestinal mucosa?
QUESTION 24
Which metabolic conversion is impaired in thiamin deficiency because of the role of thiamin diphosphate in pyruvate dehydrogenase?
QUESTION 25
A patient with thiamin deficiency develops fulminant heart failure and metabolic abnormalities without peripheral neuritis. Which syndrome best fits this presentation?
QUESTION 26
Which vitamin does not strictly meet the dietary definition of a vitamin because it can be formed from the essential amino acid tryptophan?
QUESTION 27
Which vitamin is formed in the skin from 7-dehydrocholesterol on exposure to sunlight?
QUESTION 28
Which neurological syndrome of thiamin deficiency is especially associated with alcohol and narcotic abuse?
QUESTION 29
Which enzyme is inhibited by methotrexate in cancer chemotherapy?
QUESTION 30
Which pair of compounds has the biological activity of niacin?
QUESTION 31
Which property of dihydrofolate reductase provides the basis for using its inhibitors as antibacterial and antimalarial drugs?
QUESTION 32
Which enzyme catalyzes the methylation of deoxyuridine monophosphate to thymidine monophosphate required for DNA synthesis?
QUESTION 33
How does thiamin triphosphate participate in nerve conduction?
QUESTION 34
The absence of which enzyme accounts for the dietary requirement for vitamin C in humans?
QUESTION 35
Which substance in the skin undergoes a nonenzymic reaction on ultraviolet exposure to produce previtamin D?
QUESTION 36
When one-carbon folates are not required, which process maintains a pool of free folate?
QUESTION 37
Through which pathway do animals capable of synthesizing vitamin C produce it as an intermediate?
QUESTION 38
Which one-carbon groups can bridge N-5 and N-10 of tetrahydrofolate?
QUESTION 39
Which form of rhodopsin initiates the guanine nucleotide amplification cascade during visual transduction?
QUESTION 40
In temperate climates, when is the plasma concentration of vitamin D highest?
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Study notes

Learning objectives for vitamins and dietary minerals
This passage outlines the topics to be studied but does not explain their underlying mechanisms or provide specific clinical facts. →
Biochemical functions and deficiency syndromes of vitamins and minerals
Vitamins are organic nutrients needed in small quantities for biochemical functions. They generally cannot be synthesized by the body and therefore require dietary supply. →
Determining micronutrient requirements and reference intakes
Nutrient adequacy lies between intakes that cause deficiency and intakes that exceed metabolic capacity and cause toxicity. →
Definition of vitamins and exceptions to dietary dependence
Vitamins are defined by their small dietary requirement and their role in maintaining normal metabolic integrity, although some can be formed in the body. →
Vitamin A activity: retinoids and provitamin A carotenoids
Vitamin A activity comes from preformed retinoids and from plant carotenoids that can serve as vitamin A precursors. →
β-Carotene cleavage and measures of vitamin A activity
Vitamin A content can be expressed using retinol equivalents, retinol activity equivalents, or the older international-unit system. →
Vitamin A and the visual cycle
Retinaldehyde is the prosthetic group of light-sensitive opsin proteins and is essential for initiating vision. →
Retinoic acid receptors and interaction with vitamin D and thyroid hormone signaling
Vitamin A regulates cell differentiation and turnover. Its retinoic acid forms control gene transcription through nuclear receptors. →
Vitamin A deficiency: visual progression and impaired immunity
Vitamin A deficiency is described as the most important preventable cause of blindness and also compromises immune function. →
Vitamin A toxicity: mechanism and organ manifestations
Excessive vitamin A intake can overwhelm its limited metabolic and intracellular binding capacity, causing tissue injury. →
Vitamin D: endogenous synthesis, hormonal actions, and deficiency
Vitamin D is not strictly a vitamin because it can be synthesized in the skin, which supplies most vitamin D under most conditions. →
Cutaneous synthesis and seasonal variation of vitamin D
Ultraviolet exposure initiates vitamin D synthesis from a cholesterol-synthesis intermediate that accumulates in the skin. →
Vitamin D hydroxylation in the liver and kidney
Cholecalciferol from the skin or food undergoes two hydroxylations to generate active 1,25-dihydroxyvitamin D, or calcitriol. →
Calcitriol: feedback regulation and maintenance of plasma calcium
Vitamin D controls calcium homeostasis, while its metabolism responds to factors related to plasma calcium and phosphate concentrations. →
Potential benefits and source limitations of higher vitamin D intake
The passage describes growing evidence for benefits of higher vitamin D status beyond established reference intakes. →
Skeletal effects of vitamin D deficiency
Vitamin D deficiency impairs bone mineralization in children and causes bone demineralization in adults. →
Vitamin D excess and protection against sunlight-induced toxicity
Excess dietary vitamin D can cause toxicity, and some infants develop hypercalcemia even at relatively low intakes. →
Vitamin E: membrane functions, vitamer families, and potency
Vitamin E comprises tocopherols and tocotrienols with differing biological potencies; no unequivocal unique metabolic function has been established. →
Vitamin E antioxidant action and regeneration by vitamin C
Vitamin E is a major lipid-soluble antioxidant in cell membranes and plasma lipoproteins. →
Vitamin E deficiency: impaired absorption and membrane injury
The passage distinguishes experimental animal findings from human deficiency associated with impaired vitamin absorption or transport and inadequate reserves in premature infants. →
Vitamin K: dietary forms, bacterial sources, and antagonists
Vitamin K is required for synthesis of blood-clotting proteins. Its antagonists reduce coagulation, while its biologically active forms arise from dietary, bacterial, and synthetic sources. →
Vitamin K-dependent carboxylation and the effect of warfarin
Vitamin K supports postsynthetic modification of protein glutamate residues, and its recycling explains both warfarin action and vitamin K rescue. →
γ-Carboxyglutamate in blood-clotting proteins
γ-Carboxyglutamate residues support calcium binding and membrane attachment of several proteins in the blood-clotting system. →
Vitamin K–dependent calcium-binding proteins outside coagulation
Vitamin K–dependent carboxylation of glutamate also occurs in proteins associated with bone, kidney, and regulation of cellular development and survival. →
Thiamin coenzymes in metabolism and nerve conduction
Thiamin has a central role in energy-yielding metabolism, particularly carbohydrate metabolism. Its diphosphate and triphosphate forms have distinct functions. →
Thiamin deficiency: neurological, cardiac, and metabolic effects
Thiamin deficiency produces three distinct clinical syndromes and can impair pyruvate metabolism. →
Assessment of thiamin status by erythrocyte transketolase activation
Thiamin nutritional status can be assessed using an enzyme activation procedure in erythrocyte lysate. →
Riboflavin: coenzymes, synthesis and dietary sources
Riboflavin has a central role in energy-yielding metabolism through its contribution to flavin coenzymes. →
Flavin coenzymes in oxidoreduction and oxidant stress
Flavin coenzymes act as electron carriers in metabolic oxidation reactions; their reoxidation can generate oxidant species. →
Riboflavin deficiency: conservation, manifestations, and assessment
Riboflavin is centrally involved in lipid and carbohydrate metabolism. Its deficiency occurs in many countries but is not fatal because tissue riboflavin is efficiently conserved. →
Niacin: synthesis, active forms, and metabolic function
Niacin was identified during studies of pellagra. Its synthesis from tryptophan means that it is not strictly a vitamin. →
NAD-derived ADP-ribose in DNA repair and calcium signaling
In addition to its coenzyme role, NAD supplies ADP-ribose for protein modification and gives rise to compounds involved in intracellular signaling. →
Pellagra: nutritional basis and clinical progression
Pellagra is associated with deficiency of tryptophan and niacin. Either tryptophan or niacin can prevent or cure the disease. →
Pellagra despite adequate tryptophan and niacin intake
Disease-related defects in tryptophan handling or diversion of its metabolism can cause pellagra despite an apparently adequate dietary intake. →
Adverse effects of excessive niacin intake
The passage describes adverse effects associated with nicotinic acid used for hyperlipidemia and liver toxicity from excessive intake of either niacin form. →
Vitamin B6: coenzyme forms, metabolic roles, and deficiency
Vitamin B6 functions through pyridoxal phosphate in amino acid metabolism, glycogen metabolism, and regulation of steroid hormone action. →
Vitamin B6 assessment and toxicity; vitamin B12 sources and initial absorption
This passage describes functional assessment and excess intake of vitamin B6, then introduces vitamin B12 chemistry, dietary availability, and binding proteins. →
Vitamin B12 absorption, dependent enzymes, and deficiency
This passage continues the intestinal handling of vitamin B12 and explains biochemical and hematological consequences of deficiency. →
Pernicious anemia: intrinsic factor failure and spinal cord degeneration
The target passage continues the discussion of impaired vitamin B12 absorption in pernicious anemia and explains its irreversible spinal cord complication. →
Dietary folate forms and dietary folate equivalents
Foods contain several forms of folate with differing absorption, so intake is expressed using dietary folate equivalents. →
Tetrahydrofolate carriage of one-carbon units
Tetrahydrofolate carries one-carbon fragments at specific nitrogen positions for biosynthetic reactions. →
Folate metabolism in DNA synthesis and drug action
Folate-dependent thymidine synthesis and folate regeneration provide targets for cancer chemotherapy and antimicrobial drugs. →
Vitamin B12 deficiency and the folate trap
Methionine synthase connects folate metabolism with vitamin B12 function and helps maintain tissue tetrahydrofolate availability. →
Folate deficiency and megaloblastic anemia
Actual folic acid deficiency and functional folic acid deficiency caused by vitamin B12 deficiency affect rapidly dividing cells. →
Folate supplementation: neural tube defects, homocysteine, and cancer
Folate supplementation has established effects on neural tube defects and homocysteine, while cardiovascular and cancer outcomes require careful distinction. →
Potential risks of folic acid supplementation and food enrichment
Folic acid enrichment can prevent neural tube defects, but the passage identifies groups in whom high intake may create problems. →
Biotin availability and exceptional causes of deficiency
Biotin is widely available from foods and intestinal synthesis; the passage identifies unusual circumstances in which deficiency occurs. →
Biotin in carboxylation and cell-cycle regulation
Biotin serves as a carbon dioxide carrier in a small group of carboxylase reactions. →
Pantothenic acid in coenzyme A and acyl carrier protein
Pantothenic acid participates in acyl group metabolism through its incorporation into coenzyme A and acyl carrier protein. →
Species dependence of the vitamin C requirement
Vitamin C is a dietary vitamin only in species unable to synthesize it through the uronic acid pathway. →
Vitamin C in copper- and iron-containing hydroxylases
Ascorbate supports specific hydroxylase reactions and also acts as a reducing agent and oxygen radical quencher. →
Scurvy: manifestations of vitamin C deficiency
Vitamin C deficiency causes scurvy, with manifestations attributed to impaired collagen and catecholamine synthesis. →
Higher vitamin C intake: saturation and possible benefits
The passage distinguishes saturation of vitamin C metabolism from its effects within the gut and the limited evidence concerning the common cold. →
Mineral requirements, deficiency risks and toxicity
Minerals support physiologic and biochemical functions. Adequacy depends on dietary variety, geographic food sources and losses, while excessive intake can cause toxicity. →
Vitamins and minerals: metabolic functions and deficiency
Vitamins are organic nutrients with essential metabolic functions, required in small dietary amounts because the body cannot synthesize them. Mineral elements with bodily functions must also be supplied in the diet. →
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