Human Stressors Are Driving Coastal Benthic Long-Lived Sessile Fan Mussel Pinna nobilis Population Structure More than Environmental Stressors.

Coastal degradation and habitat disruption are severely compromising sessile marine species. The fan shell Pinna nobilis is an endemic, vulnerable species and the largest bivalve in the Mediterranean basin. In spite of species legal protection, fan shell populations are declining. Models analyzed the contributions of environmental (mean depth, wave height, maximum wave height, period of waves with high energy and mean direction of wave source) versus human-derived stressors (anchoring, protection status, sewage effluents, fishing activity and diving) as explanatory variables depicting Pinna nobilis populations at a mesoscale level. Human stressors were explaining most of the variability in density spatial distribution of fan shell, significantly disturbing benthic communities. Habitat protection affected P. nobilis structure and physical aggression by anchoring reveals a high impact on densities. Environmental variables instead played a secondary role, indicating that global change processes are not so relevant in coastal benthic communities as human-derived impacts.Versión del editor4,411

Oxidative damage of rat liver mitochondria during exposure to t-butyl hydroperoxide. Role of Ca2+ ions in oxidative processes

The present study was designed for further evaluation of the biochemical mechanism of hepatic mitochondrial dysfunction under oxidative damages induced by organic hydroperoxide, tert-butyl hydroperoxide (tBHP), for estimation of the molecular targets impaired during oxidative stress, and for investigation of the role of Ca2+ ions in mitochondrial oxidative reactions and of the protective effect of melatonin during mitochondrial peroxidative damage. Main methods: Mitochondria were isolated by differential centrifugation from the rat liver. The effects of tBHP exposure, EDTA, Ca2+ ions and melatonin on mitochondrial respiratory activity, mitochondrial enzyme activities and redox status were measured. Key findings: The present study provides evidence that tBHP (at low concentrations of 0.02-0.065 mM, in EDTA-free medium) induced uncoupling of the oxidation and phosphorylation processes and decreased the efficiency of the phosphorylation reaction. This effect depended on the respiratory substrate used. The presence of EDTA prevented oxidative impairment of mitochondrial respiration, but Ca2 4 ions in the medium enhanced oxidant-induced mitochondrial damage considerably. In the presence of 0.5 mM EDTA, tBHP (at high concentrations, 0.5-2 mM) considerably oxidized mitochondrial reduced glutathione, enhanced accu¬mulation of membrane lipid peroxidation products and mixed protein-glutathione disulfides and led to an inhibition of oxoglutarate dehydrogenase and succinate dehydrogenase. Significance: Direct oxidative modification of enzymatic complexes of the respiratory chain and mitochondrial matrix, mitochondrial reduced glutathione depletion, protein glutathionylation, membrane lipid peroxidation and Ca2+ overload are the main events of mitochondrial peroxidative damages. Experiments in vitro demonstrated that melatonin inhibited the mitochondrial peroxidative damage, preventing redox-balance changes and succinate dehydrogenase inactivation

Crrections by melatonin of liver mitochondrial disorders under diabetes and acute intoxication in rats

Melatonin, disorder

Computer science. Иностранный язык

Учебно-методическое пособие.Доступ к полному тексту открыт из сети СФУ, вне сети доступ возможен для читателей Научной библиотеки СФУ или за плату.Учебно-методическое пособие включает в себя тексты по специальности и ряд упражнений грамматического и лексического характера. Предназначено для аудиторной и самостоятельной работы студентов второго курса направления 15.03.05 «Конструкторско-технологическое обеспечение машиностроительных производств»

Protective Effects of Selenopyran Against Carbon Tetrachloride Hepatotoxicity in Rats

Carbon tetrachloride (CCl4) is a known hepatotoxic compound working through the generation of reactive free radicals. Selenium (Se) is an essential trace element required by animals and humans for protection against xenobiotic compounds. In this study, Se, as selenopyran, has been evaluated for its protective action against CCl4-induced hepatotoxicity in Wistar rats. CCl4 exerts its toxic effects by generation of free radicals; it was intraperitoneally administered to male Wistar rats (2g/kg body weight) 24 h before the animals were decapitated. Selenopyran (2mg/kg body weight) was administered intragastrically one month before CCl4 injection. Rats injected with CCl4 alone showed significant lipid and hydropic dystrophy of liver, massive necrosis of hepatocytes, increases in free and conjugated bilirubin levels were marked as well as elevation of hepatic enzymes (alanine aminotransferase and aspartate aminotransferase) in plasma. Selenopyran administered at a pharmacological dose diminished the toxic effects of CCl4. Thus it decreased both the structural and functional injury of hepatocytes and clearly exerted hepatoprotective effects. These findings suggest that the effect of selenopyran on CCl4-induced acute liver injury depends on the antioxidant action Se

Protective Effects of Selenopyran Against Carbon Tetrachloride Hepatotoxicity in Rats

Protective Effects of Selenopyran Against Carbon Tetrachloride Hepatotoxicity in Rats</p