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Diabetes mellitus resulting from hyperglycemia stands as the primary cause of diabetic kidney disease. Emerging evidence suggests that plasma concentrations of soy isoflavones, substances with well-established antidiabetic properties, rise following supplemental inulin administration. The investigation encompassed 36 male Sprague–Dawley (SD) rats segregated into two cohorts: non-diabetic and diabetic, induced with type 2 diabetes (high-fat diet + two intraperitoneal streptozotocin injections). Each cohort was further divided into three subgroups (n = 6): control, isoflavone-treated, and isoflavone plus inulin-treated rats. Tail blood glucose and ketone levels were gauged. Upon termination, blood samples were drawn directly from the heart for urea, creatinine, and HbA1c/HbF analyses. One kidney per rat underwent histological (H-E) and immunohistochemical assessments (anti-AQP1, anti-AQP2, anti-AVPR2, anti-SLC22A2, anti-ACC-alpha, anti-SREBP-1). The remaining kidney underwent fatty acid methyl ester analysis. Results unveiled notable alterations in water intake, body and kidney mass, kidney morphology, fatty acids, AQP2, AVPR2, AcetylCoA, SREBP-1, blood urea, creatinine, and glucose levels in control rats with induced type 2 diabetes. Isoflavone supplementation exhibited favorable effects on plasma urea, plasma urea/creatinine ratio, glycemia, water intake, and kidney mass, morphology, and function in type 2 diabetic rats. Additional inulin supplementation frequently modulated the action of soy isoflavones. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) play in the male reproductive system important physiological functions in cell signaling, spermatogenesis and sperm maturation in epididymis. The influence of various factors, e.g. environmental, could be the reason for oxidative stress. This can lead to the exposure of cells to the toxic effects of many oxidants such as O•⁻₂, O₃, H₂O₂, •OH. The source of ROS may be spermatozoa, which also, due to the composition of the cytoplasmic membrane lipids and great amount of mitochondria are particularly susceptible to oxidative damage. Oxidative stress can damage their membranes, DNA, inhibit sperm motility and reduce their fertilization ability. This dual effect of ROS confirms the unique role of antioxidant enzymes (such as SOD, CAT and GPX) and non-enzymatic (e.g. GSH, vitamins A, E, C, transferrin) responsible for maintaining adequate levels of ROS in the male reproductive system.