Protective effect of methylene blue against copper oxide nanoparticle-induced neurobehavioral toxicity.

Increasing attention has been paid in the past decade to assessing the toxicological effects of nanoparticles and finding a protectant; thus, the current study aimed to investigate the protective effect of the mitochondria-targeting drug methylene blue (MB) against copper oxide nanoparticle (CuO-NP)-induced neurobehavioral toxicity in rats. For this purpose, twenty rats were allocated to four equal groups (n = 5). The negative control group received distilled water intraperitoneally (IP) and Tween 80 (10 %) orally. The CuO-NP group was given a dose of 100 mg/kg of CuO-NPs, administered orally, and the positive control group was treated with 1 mg/kg MB intraperitoneally (IP). The final group was concurrently exposed to CuO-NPs and MB for 14 consecutive days. At the end of the study, each group was neurobehaviorally blind tested relative to other experimental animals, then brain tissue markers were determined and a histopathological examination was conducted. The results showed that supplementation with CuO-NPs induced neurobehavioral alterations; increased Cu content in the brain; and enhanced lipid peroxidation (malondialdehyde [MDA]), protein peroxidation (protein carbonyl [PC]), and DNA oxidative damage (8-hydroxy-2-deoxyguanosine [8-OH-dG]) compared to other treatments. In addition, a decrease was noted in the mitochondrial dehydrogenases' (aldehyde dehydrogenase 2 [ALDH2], and glutamate dehydrogenase [GDH]) activity in Cu-exposed rats. The histopathological findings revealed shrunken, pyknotic, and hypereosinophic cortical neurons and increased immune positive brown staining of caspase-3 protein, indicating apoptosis. Co-treatment with methylene blue ameliorated the neurotoxic effects of CuO-NPs; therefore, MB evidently had a powerful modulatory effect against the neurotoxicity of nano-Cu oxide via its antioxidant and mitochondrial protection properties.

Effects of oral administration of aqueous extract of Fadogia agrestis (Schweinf. Ex Hiern) stem on some testicular function indices of male rats.

AIM OF THE STUDY: The effects of administration of aqueous extract of Fadogia agrestis (Schweinf. Ex Hiern) stem on some testicular function indices of male rats (Rattus norvegicus) and their recovery potentials for 10 days were investigated. MATERIALS AND METHODS: Rats were grouped into four: A, B, C and D where A (the control) received orally 1 ml of distilled water (the vehicle), B, C and D (the test groups) received orally on daily basis graded doses of 18, 50 and 100mg/kg body weight of the plant extract, respectively, for 28 days. RESULTS: Compared with the control, extract administration for 28 days at all the doses resulted in significant increase (P<0.05) in percentage testes-body weight ratio, testicular cholesterol, sialic acid, glycogen, acid phosphatase and gamma-glutamyl transferase activities while there was significant decrease (P<0.05) in the activities of testicular alkaline phosphatase, acid phosphatase, glutamate dehydrogenase and concentrations of protein. Recoveries were made by the animals on some of the testicular function indices mainly at 18 mg/kg body weight. CONCLUSIONS: The alterations brought about by the aqueous extract of Fadogia agrestis stem are indications of adverse effects on the male rat testicular function and this may adversely affect the functional capacities of the testes. The recovery made at the dose of 18 mg/kg body weight as used in folklore medicine suggests that it does not exhibit permanent toxicity at this dose.