The role of the pentose phosphate pathway in the development of metabolic disorders in the testes during rat intoxication with cypermethrin.

Cypermethrin, a synthetic pyrethroid used in crop production, veterinary medicine, and human medicine, poses a risk to human and mammalian health. The reproductive toxicity of synthetic Pyrethroids has not been fully studied, and the purpose of this study was to determine the role of the pentose phosphate pathway in the development of metabolic disorders in rat testicles during cypermethrin intoxication. The experiment was conducted on male rats, and the results showed an increase in the content of lactate, pyruvate, uric acid, inorganic phosphate (Pi) and malondialdehyde (MDA) in testicular tissue after 1-3 days. This indicates a violation of energy metabolism and increased lipid peroxidation processes, which leads to a decrease in glutathione (GSH) levels. The elevated activity of xenobiotic biotransformation systems and antioxidant enzymes exacerbates GSH depletion. Seven days after cypermethrin administration, glucose-6-phosphate dehydrogenase (G6PDH) activity decreases, and GSH deficiency becomes more pronounced. Reduced activity of enzymes of the glutathione redox cycle may be due to a deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) with inhibition of G6PDH. The low efficiency of the pentose phosphate pathway is likely due to a presumed glucose deficiency and excess lipid peroxidation products. The results of our study show that metabolic disorders that occur in the testicles during cypermethrin intoxication can lead to a decrease in the production of sex hormones and inhibition of spermatogenesis. Although sex hormone levels and spermatogenesis parameters were not directly measured in this study, the observed metabolic disruptions are consistent with previously reported impairments in steroidogenesis and spermatogenesis.