Background: Recent studies have demonstrated that many nanoparticles have an adverseor toxic effect on the kidney.Objective: To investigate the nephroprotective effect of quercetin (QT) against renal injuryinduced by titanium dioxide nanoparticles (NTiO2) in rats.Methods: NTiO2-intoxicated rats received 50 mg/kg of NTiO2 for seven days. The QT +NTiO2 group was pretreated with QT for seven days before being administered NTiO2. Uric acid,creatinine, and blood urea nitrogen were considered to be biomarkers of nephrotoxicity. Catalase(CAT) and superoxide dismutase (SOD) activities and renal levels of malondialdehyde (MDA) weremeasured to assess the oxidative stress caused by NTiO2.Results: NTiO2 significantly increased the plasma level of the biomarkers. It alsosignificantly decreased the activities of CAT (P = 0.008) and SOD (P = 0.004), and significantlyincreased the MDA levels (P = 0.007). NTiO2 caused proximal tubule damage, the accumulationof red blood cells, the infiltration of inflammatory cells, and reduced the glomerular diameters,as well as induced apoptosis in the proximal tubules. Pre-treatment with QT attenuated thehistological changes, normalised the plasma biomarkers, suppressed oxidative stress, amelioratedthe activities of CAT (P = 0.007) and SOD (P = 0.006), and reduced apoptosis (P < 0.001).Conclusion: QT was found to have a potent protective effect against nephrotoxicityinduced by NTiO2 in rats. It also reduced apoptosis caused by NTiO2.

Objective: This study investigated the effect of crocin in methylglyoxal (MGO)-induced diabetic male mice. Methods: Seventy 1-month-old male NMRI mice weighing 20–25 g were divided into seven groups (n=10): sham, MGO (600 mg/kg/day), MGO+crocin (15, 30, and 60 mg/kg/day), MGO+metformin (150 mg/kg/day), and crocin (60 mg/kg/day). MGO was administered orally for 30 days. Starting on day 14, after confirming hyperglycemia, metformin and crocin were administered orally. On day 31, plasma and tissue samples were prepared for experimental assessments. Results: Blood glucose and insulin levels in the MGO group were higher than those in the sham group (p<0.001), and decreased in response to metformin (p<0.001) and crocin treatment (not at all doses). Testis width and volume decreased in the MGO mice and improved in the crocin-treated mice (p<0.05), but not in the metformin group. Superoxide dismutase levels decreased in diabetic mice (p<0.05) and malondialdehyde levels increased (p<0.001). Crocin and metformin improved malondialdehyde and superoxide dismutase. Testosterone (p<0.001) and sperm count (p<0.05) decreased in the diabetic mice, and treatment with metformin and crocin recovered these variables. Luteinizing hormone levels increased in diabetic mice (p<0.001) and crocin treatment (but not metformin) attenuated this increase. Seminiferous diameter and height decreased in the diabetic mice and increased in the treatment groups. Vacuoles and ruptures were seen in diabetic testicular tissue, and crocin improved testicular morphology (p<0.01). Conclusion MGO increased oxidative stress, reduced sex hormones, and induced histological problems in male reproductive organs. Crocin and metformin improved the reproductive damage caused by MGO-induced diabetes.

Objective: This study investigated the effect of crocin in methylglyoxal (MGO)-induced diabetic male mice. Methods: Seventy 1-month-old male NMRI mice weighing 20–25 g were divided into seven groups (n=10): sham, MGO (600 mg/kg/day), MGO+crocin (15, 30, and 60 mg/kg/day), MGO+metformin (150 mg/kg/day), and crocin (60 mg/kg/day). MGO was administered orally for 30 days. Starting on day 14, after confirming hyperglycemia, metformin and crocin were administered orally. On day 31, plasma and tissue samples were prepared for experimental assessments. Results: Blood glucose and insulin levels in the MGO group were higher than those in the sham group (p<0.001), and decreased in response to metformin (p<0.001) and crocin treatment (not at all doses). Testis width and volume decreased in the MGO mice and improved in the crocin-treated mice (p<0.05), but not in the metformin group. Superoxide dismutase levels decreased in diabetic mice (p<0.05) and malondialdehyde levels increased (p<0.001). Crocin and metformin improved malondialdehyde and superoxide dismutase. Testosterone (p<0.001) and sperm count (p<0.05) decreased in the diabetic mice, and treatment with metformin and crocin recovered these variables. Luteinizing hormone levels increased in diabetic mice (p<0.001) and crocin treatment (but not metformin) attenuated this increase. Seminiferous diameter and height decreased in the diabetic mice and increased in the treatment groups. Vacuoles and ruptures were seen in diabetic testicular tissue, and crocin improved testicular morphology (p<0.01). Conclusion MGO increased oxidative stress, reduced sex hormones, and induced histological problems in male reproductive organs. Crocin and metformin improved the reproductive damage caused by MGO-induced diabetes.

PURPOSE: The present study was conducted to evaluate the favorable or harmful effects of betulinic acid (BA) on a diabetic reproductive system. MATERIALS AND METHODS: In this experimental study, 60 male Naval Medical Research Institute mice (20∼25 g) were randomly divided into 6 groups: control, diabetes, diabetes+BA (10, 20, and 40 mg/kg), and diabetes+ metformin (200 mg/kg). A diabetic model was induced by a single dose of streptozotocin (STZ) (65 mg/kg) injection intraperitoneally 15 minutes after an intraperitoneal administration of nicotinamide (NA) (120 mg/kg). BA and metformin were gavaged for 2 weeks after confirmed diabetes induction in the treatment groups. One day after the last treatment, plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone levels were evaluated. The cauda epididymis and testis were removed to analyze the sperm count and testis histopathology. RESULTS: LH levels increased in diabetic (p<0.001) and diabetic BA-treated mice (p=0.009). Plasma levels of testosterone (p< 0.001) and sperm count (p=0.04) decreased in these groups when compared to the control group. Furthermore, administration of 10 mg/kg (p=0.001), 20 mg/kg (p=0.004), or 40 mg/kg (p<0.001) of BA led to a greater reduction in plasma testosterone levels compared to the diabetes group. Seminiferous tubule vacuole numbers increased in diabetic and diabetic BA-treated mice, but testis morphology and FSH level assessment revealed no significant differences between the groups. CONCLUSIONS: STZ-NA can induce diabetic alterations in the male reproductive system and the administration of BA in diabetic treated mice resulted in a worse outcome.
Academies and Institutes ; Animals ; Diabetes Mellitus ; Epididymis ; Follicle Stimulating Hormone ; Humans ; Luteinizing Hormone ; Male* ; Metformin ; Mice* ; Niacinamide ; Plasma ; Seminiferous Tubules ; Sperm Count ; Spermatozoa ; Streptozocin ; Testis ; Testosterone ; Vacuoles