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Coenzyme Q10 (CoQ10), also known as decenylquinone and ubiquinone, is a quinone compound widely found in all types of cells, and its chemical name is 23-dimethoxy-5-methyl-6-decaprenylquinone. CoQ10 is a coenzyme that is not tightly bound to proteins in the respiratory chain and acts as a particularly flexible carrier between flavoproteins and cytochromes, and is an essential component of the electron transport chain for the synthesis of ATP in mitochondria. Coenzyme Q10 preparations obtained from plant and animal extracts, chemical synthesis, and microbial fermentation are widely used as energy synthesis substances in clinical practice. In addition, CoQ10 has many important physiological functions in living organisms due to its quinone and isopentenyl side chain structure. In recent years, more and more studies have found that reduced coenzyme Q10 (CoQ10H2 ubiquinol) has the ability to inhibit free radical-mediated oxidative damage to membrane lipoproteins, thus the antioxidant effect of reduced coenzyme Q10 and its role in the prevention and treatment of oxidative stress-related diseases is receiving increasing attention. The role of reduced coenzyme Q10 in the prevention and treatment of oxidative stress-related diseases is therefore receiving increasing attention.
Coenzyme Q10 is widely distributed in the human body with varying levels in the liver (60 μg-g-1), kidney (70 μg-g-1), heart (110 μg-g-1) and lowest in the lungs (8 μg-g-1). The concentration of human plasma CoQ10 ranges from 0∙75 to 1∙0 μg-ml-1, of which 75% is CoQ10H2Bowry et al. suggested that plasma CoQ10 is mostly present in combination with LDL. The total amount of Coenzyme q10 in the body ranges from 1∙0 to 1∙5 g. It is generally higher in men than in women and is mostly stored in myocytes. CoQ10 levels in the body are reported to decrease with age.
The amount of CoQ10 in the human body depends mainly on food supplementation and internal synthesis. Dietary CoQ10 is mainly derived from meat, poultry, fish and certain vegetables such as hard flowering kale and cauliflower. It is synthesized in vivo mainly from tyrosine in three main steps: synthesis of cyclic structures from tyrosine or phenylalanine; synthesis of isoprenoid from acyl CoA residues via the mevalonate bypass; and condensation within the Golgi apparatus under the action of polymerase, where the HMGCoA reductase catalyzes the reaction of the mevalonate bypass in the same way as cholesterol synthesis. Adequate vitamins such as folic acid, niacin, riboflavin and pyridoxine are also required for the synthesis process and deficiency of these nutrients will lead to insufficient CoQ10 synthesis in vivo.
Kaikkonen et al. found that sex, age, alcohol consumption, serum cholesterol, serum glutamate acyltransferase, and serum triglyceride (TG) levels were all associated with CoQ10 levels in 518 people aged 45-70 years. Mataix et al. showed that CoQ10 levels in vivo also depend on the level of oxidative stress in vivo and the saturation of fat in food. They found that different levels of dietary fat saturation led to different levels of mitochondrial coenzymes Q9 and Q10. The highest CoQ10 levels were found when polyunsaturated fatty acids were consumed; however, CoQ10 levels decreased significantly when monounsaturated fatty acids were consumed to induce a peroxidation state using adriamycin. These results suggest that when polyunsaturated fatty acids are consumed, mitochondrial membrane polyunsaturated fatty acids are increased and CoQ10 is induced to prevent the oxidation of polyunsaturated fatty acids, and when oxidative stress occurs (e.g., adriamycin-induced, food frying, excessive exercise), more CoQ10 is consumed by the oxidation of polyunsaturated fatty acids.
Coenzyme Q10 exists in both oxidized (CoQ10) and reduced (CoQ10H2) states. Only CoQ10H2 was found to have antioxidant effect. CoQ10H2 in vivo CoQ10H2 can scavenge free radicals induced by various oxidation inducers (e.g., perchlorite, lipoxygenase, transition metals, etc.) The CoQ10H2 can scavenge free radicals induced by various oxidation inducers (e.g. perchlorite, lipid oxidase, transition metals, etc.) in vivo, such as oxygen-centered radicals, carbon-centered radicals, and carbon radicals. (e.g., oxygen-centered radicals, carbon-centered radicals, singlet oxygen, etc.). CoQ10H2 reduces thiobarbitone reaction (TBRAS) and substrates (TBRAS) and conjugated dienes in vivo. CoQ10H2 has been shown to reduce the production of oxidation products such as thiobarbitone substrate (TBRAS) and conjugated dienes. It was also demonstrated that increasing the concentration of CoQ10H2 in human plasma The level of serum SOD can be increased.
The mechanism of the antioxidant effect of CoQ10H2 is not well understood. However, the current study suggests two possibilities. Most of the findings suggest that the antioxidant effect of CoQ10H2 is through the termination of free radical chain reaction and thus reducing the oxidative damage to lipids and proteins by free radicals.Frei et al. inferred the mechanism of CoQ10H2 termination of acyl radical chain reaction by using lipid-soluble free radical initiator on liposome membrane as follows.
Q10H2 + LOO. → Q10.- ＋ H+ ＋ LOOH (1)
2Q10.- + 2H+ → Q10H2 + Q10 (2)
Q10.- + H + LOO+ → Q10 + LOOH (3)
Reactions (1) to (3) are radical capture; however, the following reactions may also occur with CoQ10H2 and semi-ubiquinone Q10- radicals.
Q10 + O2 → Q10.- + 2H+ + O2.- (4)
Q10.- + O2 → Q10 + O2.- (5)
Then the superoxide radical O2.- can further oxidize CoQ10H2
Q10H2 + O2.- → Q10.- + H2O2 (6)
Reactions (4) to (6) cannot capture the radicals generated in the radical chain reaction but can reduce the amount of superoxide radicals by passively consuming CoQ10H2 to reduce their attack on lipids to trigger a new radical oxygen burst. By calculating the delay time, it is inferred that each molecule of CoQ10H2 can scavenge 1∙1 to 1∙8 radicals.
A second possible mechanism for the antioxidant effect of CoQ10 is that CoQ10H2 acts by synergizing with vitamin E. Some researchers suggest that CoQ10H2 may act by reducing the α-tocopheryl radicals produced by vitamin E during scavenging and regenerating vitamin E. Lass et al. Lass et al. in their study of the relationship between CoQ10 and α-TOH concentrations in skeletal muscle mitochondria and superoxide anion production found that the rate of superoxide anion production was higher than that of vitamin E. In their study of the relationship between superoxide anion production and mitochondrial CoQ10 and α-TOH concentrations in skeletal muscle, they found that the rate of superoxide anion production was related to α-TOH concentration but not to CoQ10 content, but an increase in CoQ10 concentration could lead to an increase in mitochondrial α-TOH content. content. Another study by this author also confirmed that CoQ10 supplementation in mice significantly increased plasma α-TO levels and found that mitochondrial α-TOH concentrations were also significantly increased. This indirectly demonstrates that CoQ10 is an important factor in the development of mitochondria. This indirectly supports the idea that CoQ10 acts through vitamin E This indirectly supports the view that CoQ10 acts through vitamin E.
However, a number of studies have confirmed that CoQ10H2 alone can act as a free radical scavenging antioxidant. It has been found that CoQ10 has a strong antioxidant capacity in vitamin E and selenium deficient states, and that endogenous CoQ10 production is enhanced in vivo in vitamin E and selenium deficient states by inducing the expression of enzymes related to endogenous CoQ10 production and increasing enzyme activity. It was also found that vitamin E supplementation without CoQ10 did not reduce the oxidative susceptibility of LDL in vitro. In an experiment using the E. coli VbiCV gene deletion model, it was found that the rate of plasma membrane superoxide anion production was twice as high in VbiCV-deficient E. coli as in the wild type, and a significant amount of superoxide anion aggregation on the plasma membrane was also significantly higher than in the wild type. Tomasetti et al. investigated whether CoQ10 affects DNA damage induced by hydrogen peroxide in lymphocytes and found that H2O2 caused a dramatic decrease in CoQ10 levels while vitamin E and ascorbic acid levels remained unchanged. The rate of DNA oxidative damage in the CoQ10-rich group was much lower than that in the control group after 30 min and was not related to the concentration of vitamin E and ascorbic acid.
Coenzyme Q10 is the main fat-soluble antioxidant in the body by scavenging free radicals and acting in synergy with vitamin E.