Impacts of engineered iron nanoparticles on oxidative stress, fatty acid composition, and histo-architecture of the smooth scallop Flexopecten glaber.

Engineered iron nanoparticles are widely used in environmental remediation, yet their potential toxic effects on marine biota remain poorly elucidated. This study aimed to gain insight into the nanoscale zero-valent iron (NZVI) toxicity mechanisms for marine invertebrates. Aside from the effect on oxidative status and histopathology, the effect of NZVI on lipid metabolism in bivalves was studied for the first time. To this end, specimens of Flexopecten glaber were exposed to ascending concentrations (0.5, 1, and 1.5 mg/L) of NZVI for 96 h. Results illustrate differential patterns of iron accumulation in the gills and the digestive gland. By increasing NZVI concentrations, the total iron level tended to markedly increase in the gills and decrease in the digestive gland, reaching 132 and 37.6 µg/g DW, respectively, in the specimens exposed to 1.5 mg/L. Biochemical and cellular biomarkers highlighted that NZVI caused oxidative stress (measured as hydrogen peroxide, malondialdehyde, and advanced oxidation protein product levels) and alterations of antioxidant defense systems, including reduced glutathione, non-protein thiol, glutathione peroxidase, superoxide dismutase, and catalase. Modulation of lipid metabolism with changed fatty acid compositions (mainly an increase in the saturation and a decrease in unsaturation levels) was also observed in both gills and digestive gland. Moreover, several histological damages, including lipofuscin accumulation, infiltrative inflammations, and digestive tubule alterations, were observed in the two studied organs, providing supplementary evidence regarding the toxic effect of NZVI. This study adds to the growing body of evidence pointing to the hazardous impacts of iron NPs on aquatic ecosystems.

Antioxidant role of selenium against maneb-induced cardiotoxicity in mice.

The current study was conducted to assess the beneficial effect of selenium (Se) on maneb-induced cardiotoxicity and fatty acid alterations in adult mice. Swiss albino male mice were assigned into four experimental groups. The first group consisted of negative controls. The second group represented the positive controls where mice received daily, via the diet, sodium selenite at a dose of 0.2 mg/kg. For the third group, mice were subjected to intraperitoneal injections of maneb (30 mg/kg BW). The fourth group (MB+Se) received daily the same dose of maneb as group 3 along with sodium selenite at the same dose as group 2. Mice exposure to maneb caused cardiotoxicity as indicated by an increase in malondialdehyde, hydrogen peroxide, and protein carbonyl levels, and an alteration of the antioxidant defense system (catalase, glutathione peroxidase, superoxide dismutase, glutathione, and vitamin C). Plasma lactate dehydrogenase activity and total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels increased, while high-density lipoprotein cholesterol level decreased. Results showed also a decrease in the amount of n-3 PUFA, docosahexaenoic, docosapentaenoic, and eicosapentaenoic acids. However, an increase in the levels of MUFA, cis-vaccenic, and palmitoleic acids was observed. Co-administration of Se restored the parameters indicated above to near control values. The histopathological findings confirmed the biochemical results. Selenium could be a useful and efficient agent against maneb-induced cardiotoxicity.