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Objective: The purpose of this study was to examine the effects of apocynin (APC), an inhibitor of NADPH oxidase (NOX), on high-fat diet (HF)-induced testis cytotoxicity. Methods: Wistar albino rats were divided into three groups as control, HF and HF+APC groups. Rats in HF and HF+APC groups were fed using HF for 16 weeks and in the last four weeks of this period vehicle solution or APC (25 mg/kg) was administered orally five days a week, respectively. Control group was fed with standart lab chow for 16 weeks. Cholesterol, triglyceride, high-density lipoproteins, leptin, estrogen, testosterone, LH and FSH were estimated in blood serum. Sperm parameters were analysed from the epididymis. Testicular malondialdehyde, 8‐hydroxy‐2‐deoxyguanosine, glutathione, superoxide dismutase and myeloperoxidase levels were estimated biochemically. Testicular morphology, proliferative, apoptotic and NOX2-positive cells were analysed histologically. HF-induced obesity caused significant alterations in serum lipid and hormone profiles. Testicular malondialdehyde, 8‐hydroxy‐2‐deoxyguanosine, and myeloperoxidase levels increased, glutathione and superoxide dismutase levels decreased in this group. Moreover, altered sperm parameters, increased degenerated seminiferous tubules, apoptotic and NOX2- positive cells and decreased proliferative cells were observed in the HF group. All these biochemical and histological alterations improved in the HF+APC group. Conclusion: HF-induced obesity causes altreations in lipid values, sperm parameters and testicular morphology by increasing oxidative stress through NOX2 activity. Apocynin might prevent testis damage via regulating oxidant/antioxidant balance.

Objective: The aim of this study was to evaluate the ameliorative effects of swimming training on renal and bladder damage caused by a highfat diet (HFD) using morphological and biochemical measurements. Methods: Sprague Dawley rats were fed either standard chow (CONT, 6% fat) or HFD (45% fat) for 18 weeks, these rats were divided into two subgroups at the last 6 weeks of the experiment. The exercise groups (CONT+EXC, HFD+EXC) were trained daily swimming sessions (1 h per day for 5 days/week) during the last 6 weeks. Kidney and bladder samples were prepared for light and electron microscopic examination at the end of experiment. Malondialdehyde, glutathione, interleukin-6, and tumor necrosis factor-α were measured by biochemically. Results: Regular morphology of the renal cortex and bladder mucosa was observed in the CONT and CONT +EXC groups. Degenerated renal corpuscles and proximal tubules in the kidney and degenerated urothelium with leaky tight junctions and mast cell increase in the bladder mucosa were observed in the HFD group. Ameliorated renal cortex and bladder mucosa were observed in the HFD+EXC group. In addition, malondialdehyde, glutathione, interleukin-6, and tumor necrosis factor-α levels were also consistent with the histological findings. Conclusion: HFD-induced renal and bladder damage may be related to increased oxidative damage. It was observed that the histological damage and altered oxidative stress parameters could be reversed by swimming training, and it is thought that moderate swimming exercise may play a role in regulating oxidative stress.