Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats.

No abstract

In the present study, it was aimed to investigate the effects of safranal, one of the components of saffron plant, on the inflammation in the rats in which experimental type 2 diabetes and obesity were formed. Type 2 diabetes is a disease characterized by insulin resistance and β-cell dysfunction. Therefore, in the present study, high-fat diet (HFD) and streptozotocin were used for being able to create experimental type 2 diabetes. In the first 6 weeks of the study, experimental groups were formed in five groups, after the stage of creating insulin resistance. The study groups were designed as control, HFD, HFD-Saf, DYB, and DYB-Saf groups. Safranal treatment was applied to the treatment groups for a period of 4 weeks. Throughout the study period (10 weeks), the weight gains and plasma glucose levels of the rats were determined each week and bi-weekly, respectively. At the end of the study, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6, tumor necrosis factor alpha (TNF-α), TAS and TOS levels in the pancreas and plasma were measured. In addition, the insulin and leptin levels in the plasma were determined. It was ascertained that, compared to the diabetic group, safranal decreased the inflammation both in the plasma and pancreas tissue, by reducing the TNF-α and IL-1β levels in particular. In addition, safranal was also found to decrease the oxidative stress increased due to type 2 diabetes in the plasma and pancreas tissue. It was concluded that safranal might be helpful in terms of reduction of diabetic complications, by means of its effects on both oxidative stress and inflammation, and that further studies should be carried out for this purpose.

The protective effect of boric acid against liver damage was evaluated by its attenuation of carbon tetrachloride (CCl(4))-induced hepatotoxicity in mice. Male albino mice were treated intraperitoneally (i.p.) with boric acid (50, 100, and 200 mg/kg) or silymarin daily for 7 days and received 0.2% CCl(4) in olive oil (10 mL/kg, i.p.) on day 7. Results showed that administration of boric acid significantly reduced the elevation in serum levels of aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase, and the level of malondialdehyde in the liver that were induced by CCl(4) in mice. Boric acid treatment significantly increased glutathione content, as well as the activities of superoxide dismutase and catalase in the liver. Boric acid treatment improved the catalytic activity of cytochrome P450 2E1 and maintained activation of nuclear factor kappa light-chain enhancer of activated B cell gene expression, with no effect on inducible nitric oxide synthase gene expression in the livers of mice. Histopathologically, clear decreases in the severity of CCl(4)-induced lesions were observed, particularly at high boric acid concentrations. Results suggest that boric acid exhibits potent hepatoprotective effects on CCl(4)-induced liver damage in mice, likely the result of both the increase in antioxidant-defense system activity and the inhibition of lipid peroxidation.

Crocin could contribute to the development of phytotherapeutic approaches in the treatment of obesity, diabetes, and diabesity (obesity-induced diabetes), which is promising as the abovementioned incidences have increased considerably in today's world.

No abstract

The therapeutic effects of melatonin or vitamin E plus Se (vE + Se) on the restrain of the heroin withdrawal-induced oxidative stress were studied. For this, rats were divided into ten groups. The rats were injected by fixed or variable doses of heroin for 16 consecutive days, and naloxone was given 1 h after the last heroin injection. One hour after naloxone administration, some groups were treated with melatonin or vE + Se. After 1 h this, blood samples were taken, and the levels of malondialdehyde (MDA) and reduced glutathione (GSH) in whole blood, ascorbic acid, α-tocopherol, retinol, β-carotene, nitrite, nitrate, and ceruloplasmin levels in the serum were measured. Our findings showed that, naloxone administration precipitated the heroin withdrawal. This also increased the level of MDA and decreased the levels of GSH in blood. Melatonin or vE + Se administration prevented the rise in MDA levels and increased the GSH levels. On the other hand, there were some significant differences between α-tocopherol, retinol, β-carotene, nitrite, nitrate, and ceruloplasmin levels of experimental groups. Results of present study showed that heroin withdrawal increased the lipid peroxidation and depressed endogenous antioxidative systems. Additionally, melatonin or vE + Se administrations prevented lipid peroxidation and augmented endogenous antioxidant defense systems.

Diabetic nephropathy is one of the most important complications of both type 1 and type 2 diabetes. The aim of this study is to investigate the curative and renal damage-reducing effects of safranal on inflammation and oxidative stress in diabetic nephropathy. Experimental type 2 diabetes was created in rats by use of high-fat diet (HFD) and streptozotocin (STZ) in the experimental animals. Safranal was then administered to two of the five experimental groups (type 2 diabetes group (DYB) and HFD groups) for a period of 4 weeks. At the end of the 10-week study, the serum blood urea nitrogen (BUN) and creatinine (CREA) levels, renal tissue oxidative stress parameters (total antioxidant capacity (TAS), total oxidant capacity (TOS), oxidative stress index (OSI), GSH, NO), and cytokine levels (TNF-α, IL-1β, IL-18, IFN-γ) were analyzed. In addition, the effect of safranal on the diabetic nephropathy-induced damage in renal tissue was also analyzed histopathologically. In this study, safranal was found to reduce dysfunction (lowered BUN and CREA levels) and tissue damage (histopathological data) that occur in renal tissue, by means of its both antioxidative and anti-inflammatory activities. In the light of these results, we suggest that safranal contributes to the development of new treatment protocols in the treatment of type 2 diabetes and its complication diabetic nephropathy.