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Table Summary of ALL COFACTORS; Origin (Vitamins), Source, Function, Deficit

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Extensive summary in table format for all Cofactors (Oxidoreductases, transferases, ligases) describing their origin (especially the VITAMIN-derived ones), Sources, Enzymes that need them, Function/ Pathway needed and Characterization/ deficit. Cofactors included: Nicotinamide Adenine Dinucleotide (NAD+/NADH), Nicotinamide Adenine Dinucleotide Phosphate (NADP+/ NADPH), Flavin Adenine Dinucleotide (FADH2), Ascorbate (Vitamin C), Dihydrobiopterin, Thiamine diphosphate (TDP), Pyridoxal Phosphate (PLP), Biotin, Tetrahydrofolate (H4F), Methylcobalamin, Deoxyadenosylcobalamin, Coenzyme A, Phosphopantetheine, Adenosine Tri-phosphate (ATP), Phosphoadenosine-Phosphosulfate (PAPS), S-adenosylmethionine (SAM) Hopefully it is of use to you :)

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Cofactors of Oxidoreductases (Transfer of 2 H or eˉ) (Generally reversible)
Origin (Vitamin) Sources Oxidized/ Reduced Co-factor Enzymes and Function/ Pathway Characterization
B3 – Niacin Meats, Beans, NAD+ / NADH+H+ Cofactor of many dehydrogenases: Deficit –rare but
Derivative of Potatoes, Yeasts, (nicotinamide adenine Pyridine dehydrogenases - catabolism of all nutrients, catabolism of Secondary: alcoholism,
pyridine: Made in the body dinucleotide) ethanol, citrate cycle, glycolysis, β-oxidation malnutrition
nicotinamide, by tryptophan NADP+ / NADPH+H+ Glucose 6-P dehydrogenase - production of NADPH in pentose cycle Advanced: Pellagra (3D
nicotinic acid catabolism (nicotinamide adenine Malic enzyme - Production of NADPH from malate disease) – Dementia,
dinucleotide phosphate) Reductases utilizing NADPH+H+ - Reducing syntheses (FA, cholesterol), Dermatitis, Diarrhea
hydroxylation (cytochrome P-450) etc.
B2 – Riboflavin Dairy product, FAD / FADH2 Cofactor of flavin dehydrogenases and oxidases: Intense yellow color
Ribitol (from ribose) whey, yeast, eggs, (flavin adenine dinucleotide) Flavin Dehydrogenases - β-oxidation of FA, citrate cycle Deficit – Inadequate
+ Flavin (derivative meat, whole grains Flavin oxidases - catabolism of AA and amines nutrition. Causes
of pteridine) Cytochromes - respiratory chain, desaturation of FA, hydroxylation cheilosis
C – Ascorbate Potatoes, fresh Dehydroascorbate/ Proline/lysine hydroxylase – synthesis of collagen, Antioxidant (reduction
fruits and Ascorbate Dopamine β-hydroxylase – synthesis of noradrenaline, of oxygen radicals and
vegetables, rose Cholesterol 7α-hydroxylase – synthesis of bile acids, free metal ions) and
hips Trimethyllysine hydroxylase – synthesis of carnitine (FA transport to regeneration of other
mitochondria), antioxidants.
p-hydroxyphenylpyruvate dioxygenase – catabolism of phenylalanine Deficit – Lack of fresh
and tyrosine fruits (Scurvy)
- Endogenous Dihydrobiopterin (BH2) / Phenylalanine hydroxylase – Hydroxylation of Aromatic AA (Phe) Deficit – Inborn defect
Derivative of synthesis de novo Tetrahydrobiopterin (BH4) Tyrosine hydroxylase – Hydroxylation of Aromatic AA (Tyr) in BH4 Synthesis,
pteridine from GTP Tryptophan Hydroxylase – Hydroxylation of Aromatic AA (Trp) Elevated phenylalanine
NO-synthase – Synthesis of NO from arginine in blood

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