Antioxidant and anti-caspase 3 effect of chitosan-Pinus merkusii extract nanoparticle against lead acetate-induced testicular toxicity in rat

Objective: To investigate the antioxidant and anti-caspase 3 effect of chitosan-Pinus merkusii extract nanoparticle on lead acetate-induced toxicity in rat testis. Methods: Chitosan-Pinus merkusii nanoparticles were identified by dynamic light scattering and scanning electron microscope. The male rats were divided into control group (rats were given with distilled water);lead acetate group [rats were injected with lead acetate 20 mg/kg body weight (BW) i.p.], and the treatment group (rats were given the chitosan-Pinus merkusii nanoparticle 150 mg;300 mg;600 mg/kg BW orally and were injected with lead acetate 20 mg/kg BW). The testis tissues were collected to evaluate the malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), histological evaluations of testis damage, and the caspase 3 mRNA expression was measured by reverse transcription-polymerase chain reaction. Results: The dynamic light scattering showed that the size of chitosan-Pinus merkusii nanoparticle was (530.2±38.2) nm. The scanning electron microscope images of the chitosan-Pinus merkusii nanoparticles showed an irregular shape, and the morphology surface showed the rough surface. The treatment with lead acetate resulted in significantly increasing MDA level and caspase 3 mRNA expression, and significantly decreasing level of SOD and GPx when compared with control group. The treatment with the chitosan-Pinus merkusii nanoparticle 600 mg/kg BW but not 150 and 300 mg/kg BW significantly decreased the MDA levels, caspase 3 mRNA expression, and also increased level of SOD and GPx when compared with lead acetate group. The lead acetate induced loss of the normal structure of testicular cells and necrosis, whereas treatment with chitosan-Pinus merkusii nanoparticle inhibited testicular cell necrosis. Conclusions: It can be concluded that chitosan-Pinus merkusii nanoparticle protects rat testis from oxidative damage and apoptosis caused by lead acetate, through increasing antioxidant and inhibiting caspase 3 expression.

Antioxidant activity of curcumine as protector on methylmercury inducedpancreas damage in mice

Curcumin has been reported to have a strong antioxidant activity. In recent years, use of antioxidant in reducing heavy metal toxicities has been increased worldwide. In this study, we investigated the protective effects of curcumin on methylmercury-induced pancreas damage in mice. Briefly, 50 male mice were divided into five groups as follows: negative control(mice were given daily with aquadest); positive control(mice were orally given 2 mg/kg BW methylmercury daily for 35 d); and the treatment groups(mice were orally adminstered with curcumin 100 mg; 200 mg; 400 mg/kg BW daily for 35 d, and from 5th day, animals were given 2 mg/kg BW methylmercury daily 1 h after curcumin administration for 30 d). On day 35, levels of glucose, insulin, MDA, SOD and GPx were measured. Pancreas also was fixed in 10% neutral buffered formalin solution for histopathological examination. The results revealed that methylmercury toxicity induced a significant increase in the levels of glucose and MDA. Moreover, a significant decrease in insulin, SOD and GPx levels was observed, and pancreas tissues showed degeneration and necrotic changes in the islets of Langerhans. Treatment with curcumin(400 mg/kg BW but not 200 mg/kg BW and 100 mg/kg BW) significantly(P<0.05) decreased glucose and MDA levels in pancreas in mercury-induced mice. Treatment with curcumin 400 mg/kg BW also significantly increased insulin, SOD and GPx levels and reversed the histopathological damage in methylmercury-induced mice. Taken together, curcumin could be a potent natural herbal product, which had pancreas protective effect against methylmercury-induced pancreas damage in mice.