Oleuropein alleviates malathion-induced oxidative stress and DNA damage in rats

The effects of acute exposure to 250 mg/kg malathion and the protective effects of 20 mg/kg oleuropein, both administered intraperitoneally, were evaluated in Wistar male rats. Malathion administration increased malondialdehyde, nitric oxide, 8-hydroxy-2′-deoxyguanosine, total oxidant status, and DNA damage, yet decreased total antioxidant activity, superoxide dismutase, and catalase activities in blood, liver, and kidney. Administration of oleuropein reversed malathion-induced oxidative stress, lipid peroxidation, DNA damage, and antioxidant enzyme activity.     

In vitro effects of lead on fatty acid composition,oxidative stress biomarkers and quality of ram spermatozoa

The sperm quality and several parameters associated with oxidative stress were evaluated in ram (Ovis aries) spermatozoa suspensions incubated with 0, 50 or 500 ng/mL Pb during 0, 1, 3 or 6 h. The presence of Pb during incubation, reduced the integrity of the acrosome, % sperm motility and integrity, and the functionality of membrane. On the contrary, % polyunsaturated fatty acids and the activities of glutathione peroxidase and superoxide dismutase in the spermatozoa suspensions were not affected by Pb. Moreover, glutathione peroxidase activity was decreased and the fatty acid composition changed due to the relative increase in % stearic acid during the incubation time independently on Pb presence. Data showed that several effects of Pb on sperm quality usually observed in vivo also occurred in vitro, but without any relationship with oxidative stress biomarkers.     

DNA damage in mouse organs and in human sperm cells by bisphenol A

Abstract

The in vivo genotoxic potential of bisphenol A using the comet assay in mice and in human sperm cells in vitro without metabolizing enzymes was studied. Male mice were exposed by oral gavage to the following doses of bisphenol A (0 125, 250 and 500?mg/kg body weight). DNA damage was investigated in liver, kidney, testes, urinary bladder, colon and lungs cells. In testicular cells, a significant increase in DNA strand breaks was observed in the lowest, but not in the medium or highest dose groups. Histopathological investigation of the testicular samples did not show any treatment dose-related effects. No DNA strand breaks were observed in any of the other investigated tissues. In human sperm cells in vitro, bisphenol A did not induce DNA strand breaks.     

Assessment of the role of thymol in combating chromium (VI)-induced oxidative stress in isolated rat erythrocytes in vitro

Thymol, the main phenolic compound in Thymus vulgaris, has been shown to have various biological effects. The main objective of this study was to investigate the efficacy of thymol on counteracting hexavalent chromium-induced oxidative damage in rat erythrocytes in vitro. The radical scavenging activity of thymol was examined using the 1, 1-diphenyl-2-picrylhydrazyl assay. Erythrocytes resistance to oxidative damage, lipid peroxidation, osmotic pressure, hemolysis as well as morphological alterations were evaluated in the presence of 2.5 µg thymol mL^?1 with or without 5 µmol hexavalent chromium mL^?1 of the incubation media. Results from the 1,1-diphenyl-2-picrylhydrazyl assay denoted good radical scavenging activity of thymol. Thymol caused a significant increase in superoxide dismutase and catalase activities and reduced glutathione content in erythrocytes intoxicated with hexavalent chromium. In contrast, the presence of thymol resulted in markedly less-elevated malondialdehyde levels, hemolysis, and destabilization of erythrocytes exposed to hexavalent chromium. Microscopically, thymol markedly reduced hexavalent chromium-induced morphological alterations in rat red blood cells. Conclusively, thymol counteracted hexavalent chromium-induced oxidative damage in rat erythrocytes.     

Cadmium sulfide nanoparticle induces oxidative stress and pro-inflammatory effects in human lung adenocarcinoma epithelial cells

Cadmium sulfide nanoparticles (CdSNP) are increasingly used in biological applications. This study was undertaken to understand the mechanisms underlying adverse effects of CdSNP using human lung adenocarcinoma epithelial (A549) cells. Cellular toxicity was evaluated by using 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide and neutral red assays. Results showed that CdSNP reduced mitochondrial function and induced lysosomal activity in concentration and time-dependent manner. CdSNP produced oxidative stress as evidenced by reduction of glutathione (GSH) levels and increase in reactive oxygen species and lipid peroxidation levels. Induction of caspase-3 enzymes and condensed, fragmented nuclei was observed in CdSNP-treated cells. Furthermore, the levels of interleukin-8, tumor growth factor and DNA fragmentation were significantly higher in CdSNP exposed cells. Data indicated that toxicity of CdSNP noted in A549 cells may be mediated through oxidative stress. This study warrants more comprehensive assessment of CdSNP prior to industrial applications.     

Nanosilica exerts cytotoxicity and apoptotic response via oxidative stress in mouse embryonic fibroblasts

Nanoscale silica is an important industrial material and extensively used in medicines. The objective of this study was to determine potential cytotoxicity and genotoxic effects attributed to nanosilica exposure in mouse embryonic fibroblasts (L929) cells. Nanosilica produced mild cytotoxicity in L929 cells. Results showed that nanosilica increased thiobarbituric acid reactive substance levels and enhanced superoxide dismutase activity but decreased levels of glutathione. This was accompanied by a concomitant generation of reactive oxygen species, loss of mitochondrial membrane potential, and activation of caspase-3 activity. In addition, in the single-cell gel test, nanosilica (50–300 μg/ml) at two treatment times 24 and 48 hr produced concentration- and time-dependent increase of DNA damage. Therefore, the obtained results indicate that nanosilica may induce genotoxic effects in cultured L929 cells associated with induction of oxidative stress.     

Effects of benzo(k)fluoranthene,a polycyclic aromatic hydrocarbon on DNA damage,lipid peroxidation and oxidative stress in marine gastropod Morula granulata

Benzo(k)fluoranthene [B(k)F] is one of the widespread priority pollutants of polycyclic aromatic hydrocarbons that has been scarcely studied for exposure assessment. With studies reporting a high amount B(k)F in sediments and water samples around the world, it has become vital to study its effects on aquatic organisms. In this connection, this study is conducted to study the effect of different concentrations of B(k)F (1, 10, 25 and 50?µg/L) in marine gastropod Morula granulata exposed in vivo for 96?h. A concentration-dependent increase in percentage tail DNA (TDNA) as measured by comet assay was observed in snails exposed to B(k)F. Exposure concentrations above 1?µg/L B(k)F showed significant increase in superoxide dismutase (SOD) activity and lipid peroxidation value in snails. After 96?h, SOD activity was found to be doubled for 50?µg/L B(k)F in comparison to control. A significant increase in catalase and glutathione S-transferase activity was observed at all exposure conditions at the end of the exposure time. Our study showed that B(k)F induces oxidative stress in snails which further lead to genotoxic damage. To our knowledge, this is the first study on oxidative stress and genotoxic damage in gastropods exposed to B(k)F.