Exploration of Cadmium Dioxide Nanoparticles on Bioaccumulation, Oxidative Stress, and Carcinogenic Potential in Oreochromis mossambicus L.

The field of nanotechnology is rapidly expanding with the advancement of novel nanopesticide and nanofertilizers that have the potential for revolutionizing applications in the agricultural industry. Here, we have done chronic toxicity of cadmium dioxide nanoparticles (CdONPs) on fish Oreochromis mossambicus (O. mossambicus) using oxidative stress and genotoxic biomarkers. In this current study, the value of LC50-96 hr of CdONPs has observed 40 µg/ml for O. mossambicus. The three sublethal concentrations, e.g., 4, 10, and 20 µg/ml were selected based on the LC50 value. The fishes were treated to the above concentration of CdONPs for 21 days and were harvested at 1, 7, 14, and 21 days for evaluation of clastogenicity, mutagenicity, and genotoxicity of NPs. Generally, significant effects (p < 0.01) were observed as a dose and duration of exposure. It was observed that lipid peroxidation (LPO) was increased and glutathione was decreased in both tissues. Micronuclei (MNi) were produced significantly in peripheral blood on 21 days at maximum concentration. A similar trend was seen in the damage of DNA with the same manner in terms of the percentage of tail DNA in the lymphocyte, gills, and kidney cells. This study explored the application oxidative stress, comet assay, and micronucleus assay for in situ aquatic laboratory studies using fish O. mossambicus for screening the ecomutagenic and genotoxic potential of environmental pollutants.

Melatonin ameliorates oxidative stress, modulates death receptor pathway proteins, and protects the rat cerebrum against bisphenol-A-induced apoptosis.

Epidemiological reports have indicated a correlation between the increasing of bisphenol-A (BPA) levels in the environment and the incidence of neurodegenerative diseases. In the present study, the protective effect of melatonin on oxidative stress and the death receptor apoptotic proteins in the cerebrum of the bisphenol-A-treated rats were examined. Adult male rats were orally administered melatonin (10mg/kg bw) concurrently with BPA (50mg/kg bw) 3 days a week for 6 weeks. BPA exposure resulted in significant elevations of oxidative stress, as evidenced by the increased malondialdehyde level and the decreased glutathione level and superoxide dismutase activity in the cerebrum. BPA caused an upregulation of p53 and CD95-Fas and activation of capsases-3 and 8, resulting in cerebral cell apoptosis. Melatonin significantly attenuated the BPA-evoked brain oxidative stress, modulated apoptotic-regulating proteins and protected against apoptosis. These data suggest that melatonin modulated important steps in the death receptor apoptotic pathway which likely related to its redox control properties. Melatonin is a promising pharmacological agent for preventing the potential neurotoxicity of BPA following occupational or environmental exposures.