Nicotine is the most toxic factor of tobacco. Genistein is a phytoestrogen and antioxidant that has numerous health benefits. The aim of this study is to evaluate the effects of genistein against toxic properties of nicotine to the pancreas of mice. For this purpose, 48 male mice were randomly assigned into six groups (n=8): normal control, nicotine control (2.5 mg/kg), genistein (25 and 50 mg/kg), and nicotine+genistein (25 and 50 mg/kg) treated groups. Various doses of genistein and genistein+nicotine were administered intraperitoneally to animals for 4 weeks. The weight of pancreas, total antioxidant capacity and nitrite oxide of serum, insulin levels, and the number and diameter of islets of Langerhans were investigated. Nicotine administration reduced significantly total antioxidant capacity, insulin, pancreas weight, and the number and diameter of islets of Langerhans and increased nitrite oxide in serum compared to the control normal group (P<0.05). Conversely, genistein and genistein+nicotine increased significantly insulin, total antioxidant capacity, and the number and diameter islets of Langerhans and decreased serum nitrite oxide compared to the nicotine control group. It seems that the genistein can improve pancreas damage following the nicotine administration.
Animals ; Genistein ; Humans ; Insulin ; Insurance Benefits ; Islets of Langerhans ; Male ; Mice ; Nicotine ; Pancreas ; Phytoestrogens ; Tobacco

OBJECTIVE: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect. G6PD plays a key role in the pentose phosphate pathway, which is a major source of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH provides the reducing equivalents for oxidation-reduction reductions involved in protecting against the toxicity of reactive oxygen species such as H₂O₂. We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of H₂O₂, which could potentially affect their motility and viability, resulting in an increased susceptibility to infertility. METHODS: Semen samples were obtained from four males with G6PD deficiency and eight healthy males as a control. In both groups, motile sperms were isolated from the seminal fluid and incubated with 0, 10, 20, 40, 60, 80, and 120 µM concentrations of H2O2. After 1 hour incubation at 37℃, sperms were evaluated for motility and viability. RESULTS: Incubation of sperms with 10 and 20 µM H₂O₂ led to very little decrease in motility and viability, but motility decreased notably in both groups in 40, 60, and 80 µM H₂O₂, and viability decreased in both groups in 40, 60, 80, and 120 µM H₂O₂. However, no statistically significant differences were found between the G6PD-deficient group and controls. CONCLUSION: G6PD deficiency does not increase the susceptibility of sperm to oxidative stress induced by H₂O₂, and the reducing equivalents necessary for protection against H₂O₂ are most likely produced by other pathways. Therefore, G6PD deficiency cannot be considered as major risk factor for male infertility.
Glucose-6-Phosphate* ; Glucosephosphate Dehydrogenase Deficiency* ; Glucosephosphate Dehydrogenase* ; Humans ; Infertility ; Infertility, Male ; Male ; NADP ; Oxidation-Reduction ; Oxidative Stress* ; Pentose Phosphate Pathway ; Reactive Oxygen Species ; Risk Factors ; Semen ; Spermatozoa*

Objective: To assess the effects of Falcaria vulgaris (F. vulgaris) as an antioxidant on damage to kidney of diabetic rats. Methods: Diabetic rats were established via streptozotocin (60 mg/kg). Various doses of F. vulgaris extracts (50, 100 and 150 mg/kg) and streptozotocin + F. vulgaris extracts were administered via intraperitoneal (i.p) injection to 48 rats (n=8 per group) for 28 d. Subsequently, ferric ion reducing antioxidant power (FRAP) of renal tissue, thiobarbituric acid reactive species, blood glucose concentrations, insulin, nitrite oxide, the weight of animals, glomeruli characteristics and kidney function were evaluated. Results: Compared with the control rats, diabetic rats showed significant increase in malondialdehyde, blood urea nitrogen, creatinine, blood glucose, nitrite oxide contents in renal tissues, and glomerular diameter. Furthermore, tissue FRAP level, body weight, number of glomeruli and plasma insulin were markedly reduced in diabetic rats when compared with the control group (P < 0.05). However, in all F. vulgaris and F. vulgaris + streptozotocin groups, malondialdehyde level, blood urea nitrogen, creatinine, glomerular diameter, nitrite oxide, and glucose levels were decreased significantly; meanwhile, tissue FRAP level, body weight, glomeruli number and insulin serum level were increased, compared to the control diabetic group (P < 0.05). Conclusions: F. vulgaris extract alleviates renal damage in diabetic rats.

BackgroundMorphine is commonly used to treat severe pain. This substance is significantly metabolized in the liver and causes disturbing effects. Genistein is an isoflavone and has antioxidant properties. The aim of this study was to evaluate the effects of genistein against morphine damages on mouse liver.

MethodsBetween May 2017 and March 2018, 48 male mice were divided into six groups (n = 8 in each group). Various doses of genistein (25 and 50 mg/kg) and morphine plus genistein (25 and 50 mg/kg) were administered intraperitoneally to 48 male mice for 20 consequent days. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), serum nitric oxide (NO) levels, liver weight, and the diameter of hepatocytes and central hepatic vein were studied and compared using one-way analysis of variance.

ResultsMorphine administration significantly increased the mean diameter of the central hepatic vein (22.76 ± 1.9 μm vs. 15.04 ± 0.60 μm, χ = 21.814, P = 0.001) and hepatocytes (3.03 ± 0.10 μm vs. 1.10 ± 0.05 μm, χ = 9.873, P = 0.001) respectively, blood serum NO level (38.00% ± 2.09% vs. 18.72% ± 4.40%, χ = 20.404, P < 0.001), liver enzyme level (AST: 111.80 ± 5.10 ng/ml vs. 81.93 ± 2.20 ng/ml, χ = 32.201, P < 0.0001; ALT: 45.14 ± 4.10 ng/ml vs. 35.49 ± 2.50 ng/ml, χ = 18.203, P < 0.0001; and ALP: 3.28 ± 0.20 ng/ml vs. 2.14 ± 0.10, χ = 5.04, P < 0.0001, respectively), and decreased liver weight (18.50 ± 0.90 g vs. 27.15 ± 0.50 g, χ = 22.415, P = 0.001) compared to saline group (0.535-0.750, P < 0.0001). However, administration of genistein plus morphine significantly enhanced liver weight (25 mg/kg: 21.15 ± 2.13 g vs. 18.50 ± 0.90 g, χ = 19.251, P < 0.0001; 50 mg/kg: 21.20 ± 1.00 g vs. 18.5 ± 0.9 g, χ = 19.502, P < 0.0001, respectively) and reduced the mean diameter of hepatocyte (25 mg/kg: 2.17 ± 0.30 μm vs. 3.03 ± 0.10 μm, χ = 22.780, P = 0.001; 50 mg/kg: 2.01 ± 0.20 μm vs. 3.03 ± 0.10 μm χ = 7.120, P = 0.001, respectively), central hepatic vein (25 mg/kg: 19.53 ± 1.00 μm vs. 22.76 ± 1.90 μm, χ = 20.681, P = 0.001; 50 mg/kg: 19.44 ± 1.20 μm vs. 22.76 ± 1.90 μm, χ = 18.451, P = 0.001, respectively), AST (25 mg/kg: 95.40 ± 5.20 ng/ml vs. 111.80 ± 5.010 ng/ml, P < 0.0001; 50 mg/kg: 90.78 ± 6.00 ng/ml vs. 111.80 ± 5.10 ng/ml, χ = 17.112, P < 0.0001, respectively), ALT (25 mg/kg: 35.78 ± 5.01 ng/ml vs. 45.14 ± 4.10 ng/ml, χ = 15.320, P < 0.0001; 50 mg/kg: 33.78 ± 2.60 ng/ml vs. 45.14 ± 4.10 ng/ml, χ = 14.023, P < 0.0001, respectively), ALP (25 mg/kg: 2.35 ± 0.30 ng/ml vs. 3.28 ± 0.20 ng/ml, χ = 4.101, P < 0.0001; 50 mg/kg: 2.34 ± 0.10 ng/ml vs. 3.28 ± 0.20 ng/ml, χ = 2.033, P < 0.0001, respectively), and NO levels (25 mg/kg: 25.92% ± 2.30% vs. 38% ± 2.09%, χ = 17.103, P < 0.0001; 50 mg/kg: 24.74% ± 4.10% vs. 38% ± 2.09%, χ = 25.050, P = 0.001, respectively) compared to morphine group.

ConclusionIt seems that genistein administration might improve liver damages induced by morphine in mice.