Antioxidant protection
Vitamin C is an important antioxidant in the aqueous environment of our body. As a “free radical scavenger”, it particularly scavenges toxic oxygen radicals, such as superoxide, hydrogen peroxide, singlet oxygen, and hydroxyl and peroxyl radicals. This prevents their penetration into the lipid system and thus lipid peroxidation. The antioxidant properties of vitamin C play an essential role in both cellular and humoral immune defense. In addition, ascorbic acid protects DNA (carrier of genetic information) from damage by reactive oxygen molecules. The antioxidant functions of L-ascorbic acid closely biochemically interact with those of vitamins A and E, as well as carotenoids.In the foreground is the ability of vitamin C to regenerate tocopherol radicals. Vitamin C present in the aqueous medium of the cytosol, with the formation of dehydroascorbic acid or by glutathione, converts vitamin E radicals previously “tipped” from the lipid phase into the aqueous phase. Subsequently, vitamin E “flips” back to the lipophilic phase to be effective again as an antioxidant.In this way, L-ascorbic acid exerts a “tocopherol-sparing effect” and supports vitamin E in its antioxidant activity.
Hydroxylation reactions
In hydroxylation reactions, vitamin C in the form of dehydroascorbic acid acts as an electron acceptor. In the form of L-ascorbic acid, on the other hand, it donates electrons or is involved in electron transfer.Hydroxylation reactions – collagen biosynthesisUse as a cofactor in collagen biosynthesis represents one of the most important biochemical functions of ascorbic acid. In collagenous connective and supportive tissue, hydroxylation of proline to hydroxyproline and of lysine to hydroxylysine occurs with the assistance of vitamin C. These protein components of collagen contribute both to its stabilization by forming a triple helix and to the formation of cross-links. Ascorbic acid is consequently essential for wound healing, scar formation, and growth (new bone, cartilage, and dentin formation).Independent of the hydroxylation reaction, L-ascorbic acid promotes collagen formation gene expression in fibroblasts. Presumably, the involvement of reactive aldehydes generated by the ascorbic acid-dependent reduction of Fe3+ (non-heme iron) to Fe2+ (heme iron) is important for this mechanism. They stimulate the transcription of collagen in fibroblasts. Furthermore, ascorbic acid supports the development and maturation of cartilage. Based on investigations, an increase in alkaline phosphatase (AP, ALP, bone-specific also ostase; is the name for enzymes that hydrolyze phosphoric acid esters) as well as a regulation of the maturing chondrocyte could be determined under the influence of ascorbic acid. Hydroxylation reactions – steroid biosynthesis L-ascorbic acid is required in hydroxylation reactions of steroids and for the formation of cholesterol-7-hydroxylase – an exceedingly necessary enzyme in the degradation of cholesterol to bile acids.The synthesis of glucocorticoids in the adrenal gland is also ascorbic acid dependent. The glucocorticoid cortisol is one of the stress hormones of the adrenal cortex and is secreted in increased amounts during situations of physical and emotional stress. Cortisol regulates salt and water balance, intervenes in protein and carbohydrate metabolism and increases fat burning. Finally, the steroid hormone contributes to energy production due to the provision of glucose and the breakdown of fat. Because cortisol also has anti-inflammatory (anti-inflammatory) and immunosuppressive effects, it is essential for coping with stress.A deficiency of ascorbic acid results in reduced glucocorticoid synthesis. Low cortisol levels ultimately lead to a reduced stress response.Hydroxylation reactions – folic acid synthesisL-ascorbic acid is involved in the conversion of folic acid to the active form – tetrahydrofolic acid – and protects the B vitamin from oxidation. Hydroxylation reactions – amino acid synthesisFurthermore, vitamin C is required for the metabolism of various amino acids, such as tryptophan, serotonin and tyrosine. The hydroxylation reaction of tryptophan to 5-hydroxytryptophan – precursor of serotonin – requires dehydroascorbic acid.Hydroxylation reactions – catecholamine biosynthesisAscorbic acid acts as a cofactor of dopamine beta-hydroxylase and is thus an essential component in the hydroxylation of dopamine to norepinephrine.During this reaction, L-ascorbic acid is oxidized to dehydroascorbic acid (DHA) with the release of hydrogen. The intermediate semidehydroascorbic acid formed in this process is converted back to ascorbic acid under the influence of the specific protein cytochrome b561, which is then available for further hydroxylation reactions.In addition to noradrenaline synthesis, ascorbic acid is also responsible for the biosynthesis of adrenaline.
Carnitine – Biosynthesis
L-carnitine is formed from the two amino acids lysine and methionine. In this chemical process, L-ascorbic acid must not be missing. The B vitamins niacin and pyridoxine are also essential for the biosynthesis of carnitine.Carnitine is needed for the introduction of long-chain fatty acids into the mitochondria and thus for energy production. When ascorbic acid stores are low, muscles lack carnitine, which can lead to disturbances in fatty acid oxidation and ultimately to weakness and fatigue.
Influence on neuroendocrine hormones
Petidylglycine-alpha-amidating monooxygenase (PAM) is an enzyme found in soluble form primarily in the pituitary gland and membranously in the atrium of the heart. With the help of L-ascorbic acid, copper and molecular oxygen, PAM catalyzes alpha-amidation.In ascorbic acid deficiency, PAM activity is decreased. As a result, alpha-amidation cannot proceed effectively. It is essential for the unfolding of the biological activity of the following peptide and neuroendocrine hormones, respectively:
- Bombesin*
- Calcitonin
- Cholecystokinin
- CRH (corticotropin-releasing hormone)
- Gastrin
- GRF (gonadotropin-releasing factor).
- TRH (thyrotropin-releasing-hormone)
- Melanotropin
- Ocytocin
- Vasopressin
Ascorbic acid occupies a special position in thyrosine metabolism. There it preserves the enzyme p-hydroxyphenylpyruvic acid hydroxylase from inhibition by its substrate. In premature infants with tyrosinemia, even small doses of ascorbic acid are sufficient to increase or normalize serum tyrosine levels.
Iron Metabolism
Phytic acid/phytates (in cereals, corn, rice, and whole grain and soy products), tannins (in coffee and tea), and polyphenols (in black tea) form a nonabsorbable complex with iron and consequently inhibit iron absorption. By attenuating their effect, ascorbic acid increases enteric iron absorption.Most importantly, the bioavailability of non-heme plant iron can be significantly increased by the simultaneous supply of ascorbic acid. By reducing Fe3+ to Fe2+, ascorbic acid improves the absorption of non-heme iron by a factor of 3-4 and stimulates its incorporation into the iron storage protein ferritin. In addition, the water-soluble vitamin increases the stability of the ferritin iron core.
Detoxification reactions
Toxic metabolites, xenobiotics-for example, herbicides, environmental toxins-and drugs are detoxified with the participation of ascorbic acid as a cofactor by the mixed-function oxidases localized in liver microsomes and the numerous hydroxylation reactions required in this process. This detoxification mechanism can be explained in the essential function of L-ascorbic acid as a free radical scavenger. L-ascorbic acid stimulates the synthesis of cytochrome P-450 dependent enzymes that detoxify toxic substances and provides protection against inactivation by oxygen radicals.Furthermore, ascorbic acid reduces the toxicity of selenium, lead, vanadium as well as cadmium. At a physiological pH of gastric juice, nitrosamines can be formed from dietary nitrite and numerous ubiquitously occurring amines, which can damage the liver and promote the formation of malignant (malignant) tumors.L-ascorbic acid is able to inhibit the formation of these hepatoxic and carcinogenic (cancer-causing) nitrosamines.
Glycolization of proteins
Glycolization of proteins is the result of the reaction of proteins (albumen) and carbohydrates or sugar molecules, which causes the two structures to stick together. These adhesions render the protein structures unusable.Of essential importance is the glycolization of hemoglobin (red blood pigment). Glycated hemoglobin – HbA1 – serves as a marker for the extent of glycolization in the body. It is useless in this form for oxygen transport in the blood and into the cell.L-ascorbic acid can reduce protein glycolization via competitive inhibition of the amino group of the protein. Thus, in diabetic patients, during three months of supplementation with 1 gram of L-ascorbic acid per day, chromatographically determined HbA1 decreased by 16% and fructosamines by 33%.Accordingly, supplementation of L-ascorbic acid may be helpful in reducing the risk of developing late diabetic damage. * Bombesin belongs to the neuroendocrine hormones or releasing hormones. As an oligopeptide – consisting of 3-14 amino acids – it is transported from the hypothalamus to the pituitary gland through the portal vasculature. Bombesin is formed in the hypothalamus (hypophyseotropic hormone) and is particularly detectable in the APUD cells of the nervous system (cells of the APUD system with the common ability to take up and decarboxylate amines or their precursors, i.e. to form polypeptide hormones) and in the duodenal mucosa (mucous membrane of the duodenum). Neurohormones stimulate the formation and secretion of glandotropic hormones in the anterior pituitary. In addition, bombesin stimulates gastric acid, gastrin, and cholecystokinin secretion.
