Beneficial effects of Salvia officinalis essential oil on vanadium-induced testicular injury, DNA damage and histological alterations in Wistar rats.

Vanadium has been shown to catalyze the generation of reactive oxygen species. Since free radical production and lipid peroxidation are potentially important mediators in testicular physiology and pathophysiology, the present study was conducted to elucidate vanadium-induced oxidative damage in rat testis and the ameliorative role of Salvia officinalis essential oil (SEO) against the adverse effects of this heavy metal. Adult male Wistar rats were treated daily during 10 days either with ammonium metavanadate (5 mg/kg bw, intraperitoneally), SEO (15 mg/kg bw, orally) or their combination. A group of rats receiving daily a saline solution served as a negative control. Vanadium treatment induced a significant decrease in body and reproductive organ weights, serum testosterone level and sperm number and motility. An increase in lipid peroxidation and protein oxidation as well as a marked inhibition in the activities of antioxidant enzymes in the testes and seminal vesicles indicated the occurrence of oxidative stress after vanadium toxicity. Histopathological changes in testis and seminal vesicles were also observed following vanadium administration. However, co-administration of SEO to vanadium-treated rats resulted in an appreciable improvement of these parameters, emphasizing the therapeutic effects of SEO. It can be suggested that SEO mitigates vanadium-induced reproductive damage due to its antioxidant capacity. Thus, we can hypothesize that SEO supplementation could protect against vanadium poisoning.

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.

Compound blue nevus: A misleading pigmented melanocytic tumor.

Compound blue nevus had clinical and histological similarities with other heavily pigmented melanocytic tumor, like the pigmented epithelioid melanocytoma. Distinctive genomic aberrations have allowed differentiating it. The defining characteristic of blue nevi family is the presence of activating mutations in the G protein α-subunits, GNAQ and GNA11.

Zinc alleviates maneb-induced kidney injury in adult mice through modulation of oxidative stress, genotoxicity, and histopathological changes.

Zinc is one of the important essential trace minerals to human health due to its antioxidant properties. The present study was conducted to elucidate its potential protective role against maneb-induced nephrotoxicity. For this purpose, animals were randomly divided into four groups of six each. Mice of group I (negative controls) have received daily 0.5 ml of distilled water, a solvent of maneb. Mice of group II (MB) have received 30 mg/kg bw of maneb daily by intraperitoneal way. Mice of group III (MB + Zn) have received the same dose of maneb as group II, along with ZnSO4 (30 mg/kg bw) daily. Mice of group IV (Zn), considered as positive controls, have received the same dose of ZnSO4 as group III daily. Our results revealed that ZnSO4 co-administration to maneb-treated mice decreased kidney levels of malondialdehyde, hydrogen peroxide, protein carbonyls, and advanced oxidation protein products; the levels of non-enzymatic antioxidants like vitamin C, glutathione, and metallothionein. It recovered the alteration of antioxidant enzyme activities (catalase, superoxide dismutase, and glutathione peroxidase) and attenuated DNA fragmentation. Furthermore, this essential trace element was also able to alleviate kidney biomarkers' alterations by lowering plasma levels of creatinine, urea, uric acid, and lactate dehydrogenase. In addition, the histopathological changes induced by maneb were improved following zinc administration. Our results indicated that zinc might be beneficial against maneb-induced renal oxidative damage in mice.