Salvia officinalis restores semen quality and testicular functionality in cadmium-intoxicated male rats.

The present study investigated the potential ability of Salvia officinalis, one of the oldest medicinal plants, to protect male rats against cadmium reproductive toxicity. Twenty-eight healthy male rats were randomly allocated into four groups (n = 7); control, Salvia-extract treated group, cadmium treated group and a group treated with both Cd and Salvia. Administration of cadmium reduced the relative testis to body weight and significantly affected sperm parameters by decreasing motility, viability, count and increasing morphological aberrations. Comet assay was used to detect DNA fragmentation in sperms of the rats exposed to Cd. Serum levels of testosterone T, follicle stimulating hormone FSH, and luteinizing hormone LH were significantly decreased. The biochemical analysis of testicular tissue showed a significant rise in Malondialdehyde MDA level coupled with a decrease in the activity of antioxidant enzymes (superoxide dismutase SOD, glutathione peroxidase GPx and catalase CAT). The histological examination of testis sections after Cd administration revealed severe degeneration of spermatogenic cells. Seminiferous tubules were filled with homogenous eosinophilic fluid associated with atrophy of other seminiferous tubules. Co-treatment with the Salvia officinalis extract restored the oxidative enzymes activities and decreased the formation of lipid peroxidation byproduct, which in turn ameliorated the effect of Cd on sperm parameters, DNA damage and testis histopathology. Taken together, it can be concluded that the synergistic antioxidant and radical savaging activities of Salvia officinalis prevented the effect of Cd on semen quality, sperm DNA damage, along with the oxidative stress and histological abnormalities in the testis tissues.

Lufenuron induces reproductive toxicity and genotoxic effects in pregnant albino rats and their fetuses.

Insecticides and other agrochemicals have become indispensable components of the agricultural system to ensure a notable increase in crop yield and food production. As a natural consequence, chemical residues result in significantly increased contamination of both terrestrial and aquatic ecosystems. The present study evaluated the teratogenic, genotoxic, and oxidative stress effects of residual-level lufenuron exposure on pregnant rats during the organogenesis gestational period of both mother and fetus. The tested dams were divided into three groups; control (untreated), low-dose group (orally administered with 0.4 mg/kg lufenuron) and high-dose group (orally administered with 0.8 mg/kg lufenuron). The dams of the two treatment groups showed teratogenic abnormalities represented by the asymmetrical distribution of fetuses in both uterine horns, accompanied by observed resorption sites and intensive bleeding in the uterine horns, whereas their fetuses suffered from growth retardation, morphologic malformations, and skeletal deformations. Histologic examination of the liver and kidney tissues obtained from mothers and fetuses after lufenuron exposure revealed multiple histopathologic changes. DNA fragmentation and cell cycle perturbation were also detected in the liver cells of lufenuron-treated pregnant dams and their fetuses through comet assay and flow cytometry, respectively. Moreover, lufenuron-induced oxidative stress in the liver of mothers and fetuses was confirmed by the increased malondialdehyde levels and decreased levels of enzymatic antioxidants (glutathione peroxidase and superoxide dismutase). Taken together, it can be concluded that lufenuron has a great potential in exerting teratogenic, genotoxic, and oxidative stresses on pregnant rats and their fetuses upon chronic exposure to residual levels during the organogenesis gestational period. The obtained results in the present study imply that women and their fetuses may have the same risk.

Evaluation of the Cytotoxicity and Apoptotic Induction in Human Liver Cell Lines Exposed to Three Food Additives.

BACKGROUND: Rapid lifestyle, especially among people living in urban areas, has led to increasing reliance on the processed food market. Unfortunately, harmful effects caused by the excessive use of food additives in such type of industry are often neglected. OBJECTIVE: This proposal investigates in vitro cytotoxic and apoptotic effects of three food preservatives commonly consumed in daily meals; sodium sulphite, boric acid, and benzoic acid. METHODS: The effect of the three preservatives on cell viability was tested on two different cell lines; normal liver cell line THLE2 and human hepatocellular carcinoma cancer cell line HepG2 using MTT assay. Cell cycle arrest was measured using flow cytometry by propidium iodide. Measurement of expression levels of two central genes, p53 and bcl-2 that play key roles in cell cycle and apoptosis was carried out in HepG2 cells using real time-PCR. RESULTS: Although the effect was more significantly realized in the HepG2 cell line, the viability of both cell lines was decreased by all of the three tested compounds. Flow cytometric analysis of HepG2 cells treated with sodium sulphite, boric acid, and benzoic acid has revealed an increase in G2/M phase cell cycle arrest. In Sodium sulphite and boric acid-treated cells, expression levels of p53 were up-regulated, while that of the Bcl2 was significantly down-regulated. On the other hand, Benzoic acid has shown an anti-apoptotic feature based on the increased expression levels of Bcl-2 in treated cells. CONCLUSION: In conclusion, all of the tested compounds have decreased the cell line viability and induced both cell cycle arrest and apoptotic events indicating their high potential of being cytotoxic and genotoxic materials.