Possible role of selenium in ameliorating lead-induced neurotoxicity in the cerebrum of adult male rats: an experimental study.

Chronic lead (Pb) poisoning is one of the greatest public health risks. The nervous system is the primary and most vulnerable target of Pb poisoning. Selenium (Se) has been shown to be a potential protection against heavy metal toxicity through anti-inflammatory and antioxidant properties. Therefore, the present study aimed to elucidate the possible protective role of Se in ameliorating the effects of Pb on rat cerebral structure by examining oxidative stress and markers of apoptosis. The rats were divided into 6 groups: control group, Se group, low Pb group, high Pb group, low Pb + Se group, high Pb + Se group. After the 4-week experiment period, cerebral samples were examined using biochemical and histological techniques. Pb ingestion especially when administered in high doses resulted in cerebral injury manifested by a significant increase in glial fibrillary acidic protein, malondialdehyde (MDA) marker of brain oxidation and DNA fragmentation. Moreover, Pb produced alteration of the normal cerebral structure and cellular degeneration with a significant reduction in the total number of neurons and thickness of the frontal cortex with separation of meninges from the cerebral surface. There was also a decrease in total antioxidant capacity. All these changes are greatly improved by adding Se especially in the low Pb + Se group. The cerebral structure showed a relatively normal histological appearance with normally attached pia and an improvement in neuronal structure. There was also a decrease in MDA and DNA fragmentation and an increase TAC. Selenium is suggested to reduce Pb-induced neurotoxicity due to its modulation of oxidative stress and apoptosis.

Naringenin alleviates hepatic injury in zinc oxide nanoparticles exposed rats: impact on oxido-inflammatory stress and apoptotic cell death.

Human exposure to nanoparticles became unavoidable secondary to their massive involvement in a multitude of industrial applications. Zinc oxide nanoparticles (ZnONPs) are one of the most commonly used metal oxide nanoparticles in biological applications. Naringenin (NAR), a citrus-derived flavonoid, has favorable biological properties that promote human health. The present study was carried out to investigate the possible defensive role of NAR versus ZnONPs provoked hepatic injury in rats through an evaluation of liver enzymes, hepatic biomarkers of oxidative stress, inflammatory process, apoptotic cell death along with histopathological examination of liver tissue. Therefore, 32 adult rats were randomly divided into four equal groups as control, NAR, ZnONPs and co-treated ZnONPs with NAR groups. All treatments were administered for 14 days. Our results showed that ZnONPs induced hepatic injury as documented by the marked increased in hepatic enzymes activities, disturbed hepatic oxidant/antioxidant balance, increased hepatic inflammatory reactions, in addition to, extensive hepatic morphological alterations, marked collagen fibers accumulation as well as overexpression of apoptotic BAX and the noticeable intensified positive nuclear staining for nuclear factor Kabba-b in hepatic tissues. Concurrent NAR supplement to ZnONPs- treated rats significantly declined liver enzymes activities, restored oxidant/antioxidant balance, reversed inflammation, induced fewer collagen fibers accumulation, and antagonized BAX-mediated apoptotic cell death in hepatic tissues. We concluded that concurrent NAR supplement to ZnONPs treated rats improved hepatic function and structure by its antioxidant, anti-inflammatory and antiapoptotic potentials.