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Alcohol Toxicity (alcohol + toxicity)
Selected AbstractsError in an Emergency Medicine Textbook: Isopropyl Alcohol ToxicityACADEMIC EMERGENCY MEDICINE, Issue 2 2002Mark Su MD No abstract is available for this article. [source] Effects of alcoholism severity and smoking on executive neurocognitive functionADDICTION, Issue 1 2009Jennifer M. Glass ABSTRACT Aims Neurocognitive deficits in chronic alcoholic men are well documented. Impairments include memory, visual,spatial processing, problem solving and executive function. The cause of impairment could include direct effects of alcohol toxicity, pre-existing cognitive deficits that predispose towards substance abuse, comorbid psychiatric disorders and abuse of substances other than alcohol. Cigarette smoking occurs at higher rates in alcoholism and has been linked to poor cognitive performance, yet the effects of smoking on cognitive function in alcoholism are often ignored. We examined whether chronic alcoholism and chronic smoking have effects on executive function. Methods Alcoholism and smoking were examined in a community-recruited sample of alcoholic and non-alcoholic men (n = 240) using standard neuropsychological and reaction-time measures of executive function. Alcoholism was measured as the average level of alcoholism diagnoses across the study duration (12 years). Smoking was measured in pack-years. Results Both alcoholism and smoking were correlated negatively with a composite executive function score. For component measures, alcoholism was correlated negatively with a broad range of measures, whereas smoking was correlated negatively with measures that emphasize response speed. In regression analyses, both smoking and alcoholism were significant predictors of executive function composite. However, when IQ is included in the regression analyses, alcoholism severity is no longer significant. Conclusions Both smoking and alcoholism were related to executive function. However, the effect of alcoholism was not independent of IQ, suggesting a generalized effect, perhaps affecting a wide range of cognitive abilities of which executive function is a component. On the other hand, the effect of smoking on measures relying on response speed were independent of IQ, suggesting a more specific processing speed deficit associated with chronic smoking. [source] Modulatory potential of ellagic acid, a natural plant polyphenol on altered lipid profile and lipid peroxidation status during alcohol-induced toxicity: A pathohistological studyJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2008Nagarajan Devipriya Abstract Polyphenol-rich dietary foodstuffs, consumed as an integral part of vegetables, fruits, and beverages have attracted attention due to their antioxidant and anticancer properties. Ellagic acid (EA), a polyphenolic compound widely distributed in fruits and nuts, has been reported to scavenge free radicals and inhibit lipid peroxidation. Chronic consumption of alcohol potentially results in serious illness including hepatitis, fatty liver, hypertriglyceridemia, and cirrhosis. A little is known about the influence of EA on alcohol toxicity in vivo. Accordingly, in the present study, we have evaluated the protective effects of EA on lipid peroxidation and lipid levels during alcohol-induced toxicity in experimental rats. Forty female albino Wistar rats, which were weighing between 150,170 g were used for the study. The toxicity was induced by administration of 20% alcohol orally (7.9 g/kg body wt.) for 45 days. Rats were treated with EA at three different doses (30, 60, and 90 mg/kg body wt.) via intragastric intubations together with alcohol. At the end of experimental duration, liver marker enzymes (i.e., aspartate transaminase, alanine transaminase), lipid peroxidative indices (i.e., thiobarbituriacid reactive substances and hydroperoxides) in plasma, and lipid levels (i.e., cholesterol, free fatty acids, triglycerides and phospholipids) in tissues were analyzed to evaluate the antiperoxidative and antilipidemic effects of EA. Liver marker enzymes, lipid peroxidative indices, and lipid levels, i.e., cholesterol, triglycerides and free fatty acids, were significantly increased whereas phospholipid levels were significantly decreased in the alcohol-administered group. EA treatment resulted in positive modulation of marker enzymes, peroxidative indices, and lipid levels. EA at the dose of 60 mg/kg body wt. was found to be more effective when compared to the other two doses. Histological changes observed were also inconsistent with the biochemical parameters. Our study suggests that EA exerts beneficial effects at the dosage of 60 mg/kg body wt. against alcohol-induced damage, and it can be used as a potential drug for the treatment of alcohol-abuse ailments in the near future. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:101,112, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20226 [source] Alcohol, Signaling, and ECM TurnoverALCOHOLISM, Issue 1 2010Devanshi Seth Alcohol is recognized as a direct hepatotoxin, but the precise molecular pathways that are important for the initiation and progression of alcohol-induced tissue injury are not completely understood. The current understanding of alcohol toxicity to organs suggests that alcohol initiates injury by generation of oxidative and nonoxidative ethanol metabolites and via translocation of gut-derived endotoxin. These processes lead to cellular injury and stimulation of the inflammatory responses mediated through a variety of molecules. With continuing alcohol abuse, the injury progresses through impairment of tissue regeneration and extracellular matrix (ECM) turnover, leading to fibrogenesis and cirrhosis. Several cell types are involved in this process, the predominant being stellate cells, macrophages, and parenchymal cells. In response to alcohol, growth factors and cytokines activate many signaling cascades that regulate fibrogenesis. This mini-review brings together research focusing on the underlying mechanisms of alcohol-mediated injury in a number of organs. It highlights the various processes and molecules that are likely involved in inflammation, immune modulation, susceptibility to infection, ECM turnover and fibrogenesis in the liver, pancreas, and lung triggered by alcohol abuse. [source] Maturation-Dependent Alcohol Resistance in the Developing Mouse: Cerebellar Neuronal Loss and Gene Expression During Alcohol-Vulnerable and -Resistant PeriodsALCOHOLISM, Issue 8 2008Bahri Karaçay Background:, Alcohol abuse during pregnancy injures the fetal brain. One of alcohol's most important neuroteratogenic effects is neuronal loss. Rat models have shown that the cerebellum becomes less vulnerable to alcohol-induced neuronal death as it matures. We determined if maturation-dependent alcohol resistance occurs in mice and compared patterns of gene expression during the alcohol resistant and sensitive periods. Methods:, Neonatal mice received alcohol daily over postnatal day (PD) 2 to 4 or PD8 to 10. Purkinje cells and granule cells were quantified on PD25. The temporal expression patterns of 4 neuro-developmental genes and 3 neuro-protective genes in the cerebellum were determined daily over PD0 to 15 to determine how gene expression changes as the cerebellum transitions from alcohol-vulnerable to alcohol-resistant. The effect of alcohol on expression of these genes was determined when the cerebellum is alcohol sensitive (PD4) and resistant (PD10). Results:, Purkinje and granule cells were vulnerable to alcohol-induced death at PD2 to 4, but not at PD8 to 10. Acquisition of maturation-dependent alcohol resistance coincided with changes in the expression of neurodevelopmental genes. The vulnerability of cerebellar neurons to alcohol toxicity declined in parallel with decreasing levels of Math1 and Cyclin D2, markers of immature granule cells. Likewise, the rising resistance to alcohol toxicity paralleled increasing levels of GABA ,-6 and Wnt-7a, markers of mature granule neurons. Expression of growth factors and genes with survival promoting function (IGF-1, BDNF, and cyclic AMP response element binding protein) did not rise as the cerebellum transitioned from alcohol-vulnerable to alcohol-resistant. All 3 were expressed at substantial levels during the vulnerable period and were not expressed at higher levels later. Acute alcohol exposure altered the expression of neurodevelopmental genes and growth factor genes when administered either during the alcohol vulnerable period or resistant period. However, the patterns in which gene expression changed varied among the genes and depended on timing of alcohol administration. Conclusions:, Mice have a temporal window of vulnerability in the first week of life, during which cerebellar neurons are more sensitive to alcohol toxicity than during the second week. Expression of genes governing neuronal maturation changes in synchrony with the acquisition of alcohol resistance. Growth factors do not rise as the cerebellum transitions from alcohol-vulnerable to alcohol-resistant. Thus, a process intrinsic to neuronal maturation, rather than rising levels of growth factors, likely underlies maturation-dependent alcohol resistance. [source] Resolution of alcoholic neuropathy following liver transplantationLIVER TRANSPLANTATION, Issue 12 2004Edward Gane Between 10 and 20% of adult liver transplants are performed for end-stage alcoholic liver disease. Severe extrahepatic end-organ damage from alcoholism (cardiomyopathy, pancreatitis, central nervous system injury, and neuropathy) is widely regarded as an absolute contraindication to liver transplantation, despite a lack of data on the effect of transplantation on these complications. We describe such a patient who presented with decompensated alcoholic liver disease and moderately severe peripheral neuropathy. Both his liver failure and neuropathy progressed despite 9 months abstinence and intensive nutritional support. By 12 months post-transplant, however, this patient had regained almost normal muscle strength, with associated recovery in sensory and motor conduction velocities. Direct alcohol toxicity, nutritional and vitamin deficiencies, and liver failure were all likely etiologic factors in this patient's neuropathy. In conclusion, this case suggests that peripheral neuropathy in a patient with alcoholic cirrhosis may resolve following liver transplantation and should not constitute a contraindication to transplantation, even when it is disabling. (Liver Transpl 2004;10:1545,1548.) [source] 24 Electrogastrography EGG in pancreas diabetesNEUROGASTROENTEROLOGY & MOTILITY, Issue 6 2006E SCHAFER Background:, Timing and criteria of testing for gastric dysmotility in pancreatic diabetes is not well established. Aim:, To investigate the pattern of EGG and autonomic neuropathy (AN) in patients with pancreas diabetes mellitus to clarify the relationship between autonomic neuropathy, alcohol consumption, glucose homeostasis, diabetes duration, and EGG. Patients and methods:, Thirty patients with pancreas diabetes mellitus were enrolled into the study. Mean duration of diabetes mellitus was 11 (0,25) years, mean blood glucose levels: 8.13 ± 2.7 mmoll,1, HbA1c 8.3 ± 2.96%; 25/30 patients were treated with insulin, the others were on rigorous diet, all of them received high dose pancreatin substitution therapy. Ten matched controls without diabetes and pancreatic insufficiency were also examined. AN was evaluated by the cardiovascular reflex tests according to the Ewing's criteria (Diab. Care 8 (5): 491,497, 1985.), EGG was monitored for 30,30 min in both fasting and in postprandial states, using a Digitrapper EGG (Synectic Med., Stockholm). EGG rhythm disturbances (bradygastria: 0,2 cpm, tachygastria: 4,10 cpm) and meal evoked EGG signal amplitude (power) changes were determined. Results:, 9/30 pts had mild to moderate parasympathetic AN, 1/30 pts had sympathetic AN, 5/30 pts had both parasympathetic and sympathetic AN; 17/30 pts demonstrated myoelectric abnormalities: 5/30 pts had predominant bradygastria, 3/30 tachygastria, and in other 9/30 pts only an absence of increase in the postprandial signal amplitude was found. Overall, 7/30 pts with abnormal EGG did not demonstrated AN. Abnormal EGG showed no correlation with actual blood sugar values or HbA1c, but it was associated with diabetes duration more than 10 years. Conclusion:, Our results suggest that beside neuropathy other factors such as alcohol toxicity, sympathetic and parasympathetic imbalance or long-term inappropriate glucose metabolism may be involved in the gastric myoelectric abnormalities provoked by pancreas diabetes. [source] Acquired loss of chromatic sensitivityACTA OPHTHALMOLOGICA, Issue 2009J BARBUR Purpose A range of ophthalmic and neurological conditions cause diminished visual performance, even when the subject is often unaware of any problems and the loss of vision remains undetected in conventional perimetry and visual acuity tests. The extent to which detection of acquired colour vision loss can revealed in subclinical cases and distinguished from congenital loss has been investigated. Methods Over 400 subjects with congenital and acquired colour vision loss have been examined using conventional colour screening methods. In addition, the loss of yellow / blue and red / green chromatic sensitivity has been quantified using the CAD test (http://www.caa.co.uk/docs/33/200904.pdf). Those investigated included subjects with diseases of the retina and / or the optic nerve as well as patients with selective damage to central visual pathways. Patients with various stages of glaucoma, photoreceptor dystrophies, diabetes, optic neuritis, age-related macular degeneration as well as tobacco and alcohol toxicity have been examined. Results Algorithms developed for analysis of colour vision loss and automatic classification of congenital and / or acquired colour deficiency will be described. In acquired deficiency, the loss of chromatic sensitivity tends to affect both the rg and the yb channels. Significant differential effects have, however, been observed in relation to stimulus size, retinal location and state of light adaptation. Conclusion The findings from these studies show that in the majority of these conditions, the loss of chromatic sensitivity is the most sensitive measure of early changes in diseases of the eye. [source] | ||||||||||