The Combined Effect of Coenzyme Q10 and Magnesium Ion on Advanced Glycation End Products Formed by Methylglyoxal in Rabbits

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Abstract

Methylglyoxal (MGO) is a poisonous and highly reactive alpha-oxoaldehyde with increased levels during oxidative stress in various disorders. MGO is generated from glyceraldehyde-3-phosphate and dihydroxyacetone phosphate during glycolysis. Continued exposure to Methylglyoxal causes Advanced Glycation End products (AGEs), implicated in different diseases, such as the early stages of diabetes, and affects male fertility, reducing sperm count and quality. This study aimed to evaluate the combined effects of coenzyme Q10 and Magnesium ion on oxidoreductase and liver enzymes due to the toxicity of MGO in experimental animals. Twenty-four rabbits (male and female) weighing 750-2100 mg, divided into four groups, were used for this experiment. Group one was used as the positive control (without treatment). Group two (negative control) received an intraperitoneal dose of 0.1 ml (20 mg/kg) per kg body weight of Methylglyoxal. Animals in group three received 0.1 ml (20 mg/kg) methylglyoxal intraperitoneally and Magnesium 5 mg/kg orally per kg body weight. Group four animals received 0.1 ml (20 mg/kg) methylglyoxal intraperitoneal, a combination of 5 mg/kg Magnesium, and 2.5 mg/kg coenzyme Q10 orally to evaluate the effect of the metal ions and antioxidants on liver enzymes activity and uric acid and other endogenous antioxidant markers (SOD and GSH). Results from our study showed that methylglyoxal exerted toxic effects on some biochemical parameters of the animals. However, the administration of CoQ10 and Magnesium ions significantly increased the levels of liver and antioxidant enzymes such as SOD and glutathione levels to resist oxidative overload.

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Saber, B. K., Ramadhan, U. H., & Abdulkareem, Q. (2022). The Combined Effect of Coenzyme Q10 and Magnesium Ion on Advanced Glycation End Products Formed by Methylglyoxal in Rabbits. Tropical Journal of Natural Product Research, 6(10), 1602–1606. https://doi.org/10.26538/tjnpr/v6i10.7

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