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The present invivo study was designed to elucidate the toxic effect of lead on oxidative stress, Na(+)K(+)ATPase and mitochondrial electron transport chain activity of the brain of Clarias batrachus. The fish were exposed to 10 and 20% of the derived 96 h LC(50) value, 37.8 and 75.6 mg L(-1), respectively, and sampled on 20, 40 and 60 days. Exposure of fish brain to lead demonstrated an increased production of reactive oxygen species, increased lipid peroxidation, loss of protein thiol groups in synaptosomal fraction with the decreased activity of Na(+)K(+)ATPase, partial inactivation of mitochondrial electron transport chain activity and energy depletion. However, no change in protein carbonyl content in synaptosomal fraction was observed due to lead exposure. Concluding the results of our investigation we suggest that lead exposure induces oxidative stress in the brain of Clarias batrachus and the decline in Na(+)K(+)ATPase activity was presumeably mediated by the combined action of lipid peroxidation and deficient mitochondrial electron transport chain activity.

Static renewal bioassays were conducted in the laboratory and in outdoor artificial enclosures to evaluate toxic effects of methanol to one teleost fish and two aquatic invertebrates and to limnological variables of aquatic ecosystem. Ninety-six-hour acute toxicity tests revealed cladoceran crustacea Moina micrura as the most sensitive to methanol (LC50, 4.82 g/L), followed by freshwater teleost Oreochromis mossambicus (LC50, 15.32 g/L) and oligochaete worm Branchiura sowerbyi (LC50, 54.89 g/L). The fish, when exposed to lethal concentrations of methanol, showed difficulties in respiration and swimming. The oligochaete body wrinkled and fragmented under lethal exposure of methanol. Effects of five sublethal concentrations of methanol (0, 23.75, 47.49, 736.10, and 1527.60 mg/L) on the feeding rate of the fish and on its growth and reproduction were evaluated by separate bioassays. Ninety-six-hour bioassays in the laboratory showed significant reduction in the appetite of fish when exposed to 736.10 mg/L or higher concentrations of methanol. Chronic toxicity bioassays (90 days) in outdoor enclosures showed a reduction in growth, maturity index and fecundity of fish at 47.49 mg/L or higher concentrations of methanol. Primary productivity, phytoplankton population, and alkalinity of water were also reduced at these concentrations. Chronic exposure to 1527.60 mg/L methanol resulted in damages of the epithelium of primary and secondary gill lamellae of the fish. The results revealed 23.75 mg/L as the no-observed-effect concentration (NOEC) of methanol to freshwater aquatic ecosystem.

Lead (Pb) is one of the most pollutant metals that accumulate in the brain mitochondria disrupting mitochondrial structure and function. Though oxidative stress mediated by reactive oxygen species remains the most accepted mechanism of Pb neurotoxicity, some reports suggest the involvement of nitric oxide (NO) and reactive nitrogen species in Pb-induced neurotoxicity. But the impact of Pb neurotoxicity on mitochondrial respiratory enzyme complexes remains unknown with no relevant report highlighting the involvement of peroxynitrite (ONOO) in it. Herein, we investigated these effects in in vivo rat model by oral application of MitoQ, a known mitochondria-specific antioxidant with ONOO scavenging activity. Interestingly, MitoQ efficiently alleviated ONOO-mediated mitochondrial complexes II, III and IV inhibition, increased mitochondrial ATP production and restored mitochondrial membrane potential. MitoQ lowered enhanced caspases 3 and 9 activities upon Pb exposure and also suppressed synaptosomal lipid peroxidation and protein oxidation accompanied by diminution of nitrite production and protein-bound 3-nitrotyrosine. To ascertain our in vivo findings on mitochondrial dysfunction, we carried out similar experiments in the presence of different antioxidants and free radical scavengers in the in vitro SHSY5Y cell line model. MitoQ provided better protection compared to mercaptoethylguanidine, N-nitro-L-arginine methyl ester and superoxide dismutase suggesting the predominant involvement of ONOO compared to NO and O. However, dimethylsulphoxide and catalase failed to provide protection signifying the noninvolvement of OH and HO in the process. The better protection provided by MitoQ in SHSY5Y cells can be attributed to the fact that MitoQ targets mitochondria whereas mercaptoethylguanidine, N-nitro-L-arginine methyl ester and superoxide dismutase are known to target mainly cytoplasm and not mitochondria. Taken together the results from the present study clearly brings out the potential of MitoQ against ONOO-induced toxicity upon Pb exposure indicating its therapeutic potential in metal toxicity.

, characterization and antimicrobial activity of some nickel, cadmium and mercury complexes of 5-methyl-3yl-N-(2´-methylthiophenyl)methyleneimine, (MP z OATA) ligand

Steady state and stability characteristics of hydrostatic two-layered porous oil journal bearings are obtained. The governing differential equations are solved numerically using the finite difference method for a wide range of design parameters. The effects of the eccentricity ratio, slenderness ratio, bearing number, feeding parameter and anisotropy of permeability on the load-carrying capacity, attitude angle, friction variable and oil flowrate have been investigated. Stability analysis has been performed using the linearized perturbation method. It has been observed that a two-layered porous bearing gives higher stability than a single-layered porous bearing.

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