973 resultados para Biochemical effects of ethanol


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The present study dealt with the haematological, biochemical and istopathological impacts of different sub lethal concentrations of ethanol on a euryhaline teleost Oreochromis In05.sambicu.5' (Peters).Studies carried out using GC indicated an increase in blood ethanol oncentration of the fish which mainly arose due to fishes entering into a state of hypoxia which explains ethanol production as an ubiquitous anaerobic end product, which gets accumulated whenever metabolic demand exceeds the mitochondrial oxidative potential. The very low amount of ethanol detected in the control group ofO mossambicns was mainly due to the activity of microorganisms in the gut ofO. Nzossambicus.Oedcma observed in the present study, is a defense mechanism that reduces the branchial superficial area of the fish which comes in contact with the external milieu. These mechanisms also increase the diffusion barrier to the pollutant. Dilation of the blood vessels is due to increased permeability helping in the free passage of ethanol into the blood stream. Telangiectasis observed explains the state of asphyxia of the fish when subjected to ethanol toxicity indicating acute respiratory distress. Gill aneurysm observed indicates impaired respiratory function. This is related to the rupture of the pillar cells which results in an increased blood flow inside the lamellae, causing dilation of the blood vessel or even aneurysm of gill.The present findings warrant future studies to explore A'T'Pases as possible biomarkers of pollutant exposure in ecotoxicology. This study indicated that O. mossambicus when exposed for 7 and 21 days to ethanol was under tremendous stress and parameters employed in this study can be adapted for future investigations as biomarkers of damage caused by ethanol to aquatic organisms. The present study revealed that O. mossambicus is sensitive to sub lethal concentrations of ethanol.

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Alcohol use disorders (AUDs) are a major public health problem, and the few treatment options available to those seeking treatment offer only modest success rates. There remains a need to identify novel targets for the treatment of AUDs. The neuronal nicotinic acetylcholine receptors (nAChRs) represent a potential therapeutic target in the brain, as recent human genetic studies have implicated gene variants in the 5 nAChR subunit as high risk factors for developing alcohol dependence. Here, we evaluate the role of 5* nAChR for ethanol-mediated behaviors using 5+/+ and 5-/- mice. We characterized the effect of hypnotic doses of ethanol and investigated drinking behavior using an adapted Drinking-in-the Dark (DID) paradigm that has been shown to induce high ethanol consumption in mice. We found the 5 subunit to be critical in mediating the sedative effects of ethanol. The 5-/- mice showed slower recovery from ethanol-induced sleep, as measured by loss of righting reflex. Additionally the 5-/- mice showed enhanced impairment to ethanol-induced ataxia. We found the initial sensitivity to ethanol and ethanol metabolism to be similar in both 5+/+ and 5-/- mice. Hence the enhanced sedation is likely due to a difference in the acute tolerance of ethanol in mice deficient of the 5 subunit. However the 5 subunit did not play a role in ethanol consumption for ethanol concentrations ranging from 5% to 30% in the DID paradigm. Additionally, varenicline (Chantix) was effective in reducing ethanol intake in 5-/- mice. Together, our data suggest that the 5 nAChR subunit is important for the sedative hypnotic doses of ethanol but does not play a role in ethanol consumption. Varenicline can be a treatment option even when there is loss of function of the 5 nAChR subunit.

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3,5-Diethoxycarbonyl-1,4-dihydrocollidine (DDC) is a porphyrinogenic agent and is a powerful inducer of -aminolaevulinate synthetase, the first and rate-limiting enzyme of the haem-biosynthetic pathway, in mouse liver. However, DDC strikingly inhibits mitochondrial as well as microsomal haem synthesis by depressing the activity of ferrochelatase in vivo. The drug on repeated administration to female mice has been found to elicit hypertrophic effects in the liver microsomes initially, but the effects observed at later stages denote either hyperplasia or increase in polyploidal cells. The microsomal protein concentration shows a striking decrease with repeated doses of the drug. The rate of microsomal protein synthesis in vivo as well as in vitro shows an increase with two injections of DDC but decreases considerably with repeated administration of the drug. The activities of NADPH-cytochrome creductase and ribonuclease are not affected in the liver microsomes of drug-treated animals when expressed per mg of microsomal protein. DDC has also been found to cause degradation of microsomal haem, which is primarily responsible for the decrease in cytochrome P-450 content. The drug also leads to a decrease in mitochondrial cytochrome c levels due to inhibition of haem synthesis and also due to degradation of mitochondrial haem at later stages. The biochemical effects of the drug are compared and discussed with those reported for allylisopropylacetamide and phenobarbital.

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Successive administrations of allylisopropylacetamide, a potent porphyrinogenic drug, increase liver weight, microsomal protein and phospholipid contents. There is an increase in the rate of microsomal protein synthesis in vivo and in vitro. The drug decreases microsomal ribonuclease activity and increases NADPHcytochrome c reductase activity. Phenobarbital, which has been reported to exhibit all these changes mentioned, is a weaker inducer of -aminolaevulinate synthetase and increases the rate of haem synthesis only after a considerable time-lag in fed female rats, when compared with the effects observed with allylisopropylacetamide. Again, phenobarbital does not share the property of allylisopropylacetamide in causing an initial decrease in cytochrome P-450 content. Haematin does not counteract most of the biochemical effects caused by allylisopropylacetamide, although it is quite effective in the case of phenobarbital. Haematin does not inhibit the uptake of [2-14C]allylisopropylacetamide by any of the liver subcellular fractions.

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Successive administrations of allylisopropylacetamide, a potent porphyrinogenic drug, increase liver weight, microsomal protein and phospholipid contents. There is an increase in the rate of microsomal protein synthesis in vivo and in vitro. The drug decreases microsomal ribonuclease activity and increases NADPH-cytochrome c reductase activity. Phenobarbital, which has been reported to exhibit all these changes mentioned, is a weaker inducer of delta-aminolaevulinate synthetase and increases the rate of haem synthesis only after a considerable time-lag in fed female rats, when compared with the effects observed with allylisopropylacetamide. Again, phenobarbital does not share the property of allylisopropylacetamide in causing an initial decrease in cytochrome P-450 content. Haematin does not counteract most of the biochemical effects caused by allylisopropylacetamide, although it is quite effective in the case of phenobarbital. Haematin does not inhibit the uptake of [2-(14)C]allylisopropylacetamide by any of the liver subcellular fractions.

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Bioethanol is the world's largest-produced alternative to petroleum-derived transportation fuels due to its compatibility within existing spark-ignition engines and its relatively mature production technology. Despite its success, questions remain over the greenhouse gas (GHG) implications of fuel ethanol use with many studies showing significant impacts of differences in land use, feedstock, and refinery operation. While most efforts to quantify life-cycle GHG impacts have focused on the production stage, a few recent studies have acknowledged the effect of ethanol on engine performance and incorporated these effects into the fuel life cycle. These studies have broadly asserted that vehicle efficiency increases with ethanol use to justify reducing the GHG impact of ethanol. These results seem to conflict with the general notion that ethanol decreases the fuel efficiency (or increases the fuel consumption) of vehicles due to the lower volumetric energy content of ethanol when compared to gasoline. Here we argue that due to the increased emphasis on alternative fuels with drastically differing energy densities, vehicle efficiency should be evaluated based on energy rather than volume. When done so, we show that efficiency of existing vehicles can be affected by ethanol content, but these impacts can serve to have both positive and negative effects and are highly uncertain (ranging from -15% to +24%). As a result, uncertainties in the net GHG effect of ethanol, particularly when used in a low-level blend with gasoline, are considerably larger than previously estimated (standard deviations increase by >10% and >200% when used in high and low blends, respectively). Technical options exist to improve vehicle efficiency through smarter use of ethanol though changes to the vehicle fleets and fuel infrastructure would be required. Future biofuel policies should promote synergies between the vehicle and fuel industries in order to maximize the society-wise benefits or minimize the risks of adverse impacts of ethanol.

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The biochemical effects of gadolinium chloride were studied using high-resolution H-1 nuclear magnetic resonance (NMR) spectroscopy to investigate the biochemical composition of tissue (liver and kidney) aqueous extracts obtained from control and gadolinium chloride (GdCl3) (10 and 50 mg/kg body weight, intraperitoneal injection. i.p.) treated rats. Tissue samples were collected at 48, 96 and 168 h p.d. after exposure to GdCl3, and extracted using methanol/chloroform solvent system. H-1 NMR spectra of tissue extracts were analyzed by pattern recognition using principal components analysis. The liver damages caused by GdCl3 were characterized by increased succinate and decreased glycogen level and elevated lactate, alanine and betaine concentration in liver. Furthermore, the increase of creatine and lactate, and decrease of glutamate, alanine, phosphocholine, glycophosphocholine (GPC), betaine, myo-inositol and trimethylamine N-oxide (TMAO) levels in kidney illustrated kidney disturbance induced by GdCl3.

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Pattern recognition methods were applied to the analysis of 600 MHz H-1 NMR spectra of urine from rats dosed with compounds that induced organ-specific damage in the liver and kidney. Male Wistar rats were separated into groups (n=4) and each was treated with one of following compounds: HgCl2, CCl4, Lu(NO3)(3) and Changle (a kind of rare earth complex mixed with La, Ce, Pr and Nd). Urine samples from the rats dosed with HgCl2, CCl4 and Lu(NO3)(3) were collected over a 24 h time course and the samples from the rats administrated with Changle were gained after 3 months. These samples were measured by 600 MHz NMR spectroscopy. Each spectrum was data-processed to provide 223 intensity-related descriptors of spectra. Urine spectral data corresponding to the time intervals, 0-8 h (HgCl2 and CCl4), 4-8 (Lu(NO3)(3)) h and 90 d (Changle) were analyzed using principal component analysis (PCA). Successful classification of the toxicity and biochemical effects of Lu(NO3)(3) was achieved.

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High resolution magic angle spinning (MAS)-H-1 nuclear magnetic resonance (NMR) spectroscopic-based metabonomic approach was applied to the investigation on the acute biochemical effects of Ce(No-3)(3). Male Wistar rats were administrated with various doses of Ce (NO3)(3)(2, 10, and 50 mg(.)kg(-1) body weight), and MAS H-1 NMR spectra of intact liver and kidney tissues were analyzed using principal component analysis to extract toxicity information. The biochemical effects of Ce (NO3)(3) were characterized by the increase of triglycerides and lactate and the decrease of glycogen in rat liver tissue, together with an elevation of the triglyceride level and a depletion of glycerophosphocholine and betaine in kidney tissues. The target lesions of Ce (NO3)(3) on liver and kidney were found by MAS NMR-based metabonomic method. This study demonstrates that the combination of MAS H-1 NMR and pattern recognition analysis can be an effective method for studies of biochemical effects of rare earths.

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The problems of relating the results of experiments in the laboratory to events in nature are twofold: to equate the response to a single variable (hydrocarbons) with the natural variability in the biological material in a multivariate environment, and to consider whether the response established experimentally has any relevance to the animal's chances of survival and reproduction (i.e. its fitness) in the natural population. Recent studies of the effects of petroleum hydrocarbons on marine invertebrates are reviewed, with an emphasis on the physiological and cytochemical responses by bivalve molluscs. The dose-response relations that emerge suggest the intensity of the 'signal' that must be detected in nature if the chronic, sublethal effects of petroleum pollution are to be measured. The natural variability in these physiological and cytochemical processes are then reviewed and the main causes of variability in natural populations, both endogenous and exogenous, discussed. These results indicate the extent of the `noise' above which the signal from possible pollution effects must be detected. The results from recent field studies on the common mussel, Mytilus edulis, are discussed. The results are as complex as expected, but it proves possible to reduce the variance in the measured responses so that pollution effects, including those due to hydrocarbons, can be detected. The ecological consequences of the observed effects of petroleum hydrocarbons are then discussed in terms of reproductive effort and reproductive value. Considerable variation between populations exists here also and this can be used to help in the interpretation of the extent of the impact of the environment on the ecology of the population. The result is to place the findings of the laboratory experiments in an ecological context of natural variability and of the physiological costs of adaptation.

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The present work is a base line attempt to investigate and assess the toxicities of three surfactants viz. anionic sodium dodecyl sulfate (SDS), non ionic Triton X-1OO (TX-IOO) and cationic cetyl trimethyl ammonium bromide (CTAB). These compounds represent simple members of the often neglected group of aquatic pollutants i.e. the anionic alkyl sulfates, non ionics and the cationics. These compounds are widely used In plastic industry, pesticide/herbicide formulations, detergents, oil spill dispersants, molluscicides etc. The test organisms selected for the present study are the cyanobacterium Synechocystis salina Wislouch representing a primary producer in the marine environment and a fresh water adapted euryhaline teleost Oreochromis mossambicus (peters) at the consumer level of the ecological pyramid. The fish species, though not indigenous to our country, is now found ubiquitously in fresh water systems and estuaries. Also it is highly resistant to pollutants and has been suggested as an indicator of pollution in tropical region .

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Dept.of Marine Biology,Microbiology & Biochemistry,Cochin University of Science and Technology

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Man uses a variety of synthetic material for his comfortable materialistic life. Thus human interactions may become harmful for various terrestrial and aquatic lives. This is by contaminating their habitat and by becoming a threat to organisms itself. Thus the application and dispersal of several organic pollutants can lead to the development of several mutated forms of the species when exposed to sublethal concentrations of the pollutants. Otherwise, a decrease in number or extinction of these exposed species from earth's face may happen. Pesticides, we use for the benefit of crop yield, but its persistence may become havoc to non-target organism. Pesticides reaching a reservoir can subsequently enter the higher trophic levels. Organophosphorus compounds have replaced all other pesticides, due to its acute toxicity and non-persistent nature.Hence the present study has concentrated on the toxicity of the largest market-selling and multipurpose pesticide, chlorpyrifos on the commonly edible aquatic organism, fish. The euryhaline cichlid Oreochromis mossambicus was selected as animal model. The study has concentrated on investigating biochemical parameters like tissue-specific enzymes, antioxidant and lipid-peroxidation parameters, haematological and histological observations and pesticide residue analysis.Major findings of this work have indicated the possibility of aquatic toxicity to the fish on exposure to the insecticide chlorpyrifos. The insecticide was found as effective to induce structural alteration, depletion in protein content, decrease in different metabolic enzyme levels and to progress lipid peroxidation on a prolonged exposure of 21 days. The ion-transport mechanism was found to be adversely affected. Electrophoretic analysis revealed the disappearance of several protein bands after 21days of exposure to chlorpyrifos. Residue, analysis by gas chromatography explored the levels of chlorpyrifos retaining on the edible tissue portions during exposure period of 21days and also on a recovery period of 10 days.

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The present work is a base|ine attempt to investigate and assess the toxicity of water-accommodated fractions (WAF) of Bombay High crude oil. The experimental animal selected for the present study is a euryhaline teleost, Oreochromis mossambicus (Peters), adapted to fresh water. The fish has been selected on account of its economic valve, abundant availability, experimental feasibility, ease of rearing and maintenance and also because it is one of the commonly cultured species in the South-East Asian countries.