scholarly journals Long-Term Ethanol Consumption Leadsto Lung Tissue Oxidative Stress and Injury

2010 ◽  
Vol 3 (6) ◽  
pp. 414-420 ◽  
Author(s):  
Subir Kumar Das ◽  
Sukhes Mukherjee

Background: Alcohol abuse is a systemic disorder. The deleterious health effects of alcohol consumption may result in irreversible organ damage. By contrast, there currently is little evidence for the toxicity of chronic alcohol use on lung tissue. Hence, in this study we investigated long-term effects of ethanol in the lung.Results: Though body weight of rats increased significantly with duration of exposure compared to its initial weight, there was no significant change in relative weight (g/100 g body weight) of lung due to ethanol exposure. The levels of thiobarbituric acid reactive substances (TBARS), nitrite, protein carbonyl, oxidized glutathione (GSS G), redox ratio (GSS G/ GSH ) and GST activity elevated; while reduced glutathione (GSH ) level and activities of glutathione reductase (GR), glutathione peroxidase (GPx), catalase, superoxide dismutase (SOD) and Na+K+ATPase reduced significantly with duration of ethanol exposure in the lung homogenate compared to the control group. Total matrix metalloproteinase activity elevated in the lung homogenate with time of ethanol consumption. Histopathologic examination also demonstrated that severity of lung injury enhanced with duration of ethanol exposure.Methods: 16–18 week-old male albino Wistar strain rats weighing 200–220 g were fed with ethanol (1.6 g/kg body weight/day) up to 36 weeks. At the end of the experimental period, blood samples were collected from reteroorbital plexus to determine blood alcohol concentration and the animals were sacrificed. Various oxidative stress-related biochemical parameters, total matrix metalloproteinase activity and histopathologic examinations of the lung tissues were performed.Conclusions: Results of this study indicate that long-term ethanol administration aggravates systemic and local oxidative stress, which may be associated with lung tissue injury.

Author(s):  
Antoniette M. Maldonado-Devincci ◽  
Joseph G. Makdisi ◽  
Andrea M. Hill ◽  
Renee C. Waters ◽  
Nzia I. Hall ◽  
...  

AbstractWith alcohol readily accessible to adolescents, its consumption leads to many adverse effects, including impaired learning, attention, and behavior. Adolescents report higher rates of binge drinking compared to adults. Adolescents are also more prone to substance use disorder during adulthood due to physiological changes during the adolescent developmental period. We used C57BL/6J male and female mice to investigate the long-lasting impact of binge ethanol exposure during adolescence on voluntary ethanol intake and open field behavior during later adolescence and in young adulthood. The present set of experiments were divided into four stages: (1) chronic intermittent vapor inhalation exposure, (2) abstinence, (3) voluntary ethanol intake, and (4) open field behavioral testing. During adolescence, male and female mice were exposed to air or ethanol using an intermittent vapor inhalation with repeated binge pattern ethanol exposure from postnatal day (PND) 28–42. Following this, mice underwent abstinence during late adolescence from PND 43–49 (Experiment 1) or PND 43–69 (Experiment 2). Beginning on PND 49–76 (Experiment 1) or PND 70–97 (Experiment 2), mice were assessed for intermittent voluntary ethanol consumption using a two-bottle drinking procedure over 28 days. Male mice that were exposed to ethanol during adolescence showed increased ethanol consumption during later adolescence (Experiment 1) and in emerging adulthood (Experiment 2), while the female mice showed decreased ethanol consumption. These data demonstrate a sexually divergent shift in ethanol consumption following binge ethanol exposure during adolescence and differences in open field behavior. These data highlight sex-dependent vulnerability to developing substance use disorders in adulthood.Significance StatementCurrently, it is vital to determine the sex-dependent impact of binge alcohol exposure during adolescence, given that until recently females have largely been ignored. Here we show that adolescent male mice that are exposed to binge ethanol during adolescence show long-term changes in behavior in adulthood. In contrast, female mice show a transient decrease in ethanol consumption in adulthood and decreased motor activity spent in the center zone of the open field test. Male mice appear to be more susceptible to the long-term changes in ethanol consumption following binge ethanol exposure during adolescence.


1999 ◽  
Vol 276 (2) ◽  
pp. H464-H471 ◽  
Author(s):  
Mika Kähönen ◽  
Kirsi Karjala ◽  
Nina Hutri-Kähönen ◽  
Xiumin Wu ◽  
Pia Jaatinen ◽  
...  

The aim of this work was to evaluate the effects of long-term ethanol consumption on arterial responses in vitro in young and aged rats. Therefore, Wistar rats (ages 3 and 29 mo, respectively) were allocated to six groups: control-young, sucrose-young, ethanol-young, control-aged, sucrose-aged, and ethanol-aged. The ethanol-fed groups were given 25% ethanol by intragastric gavage three times a day 4 days a week. Responses of mesenteric arterial rings were examined in standard organ chambers after 5 treatment weeks. In norepinephrine-precontracted arterial rings, endothelium-dependent relaxations to acetylcholine, as well as endothelium-independent relaxations to isoproterenol, were attenuated in aged rats when compared with young controls. Relaxation responses to isoproterenol, but not to acetylcholine and nitroprusside, were clearly improved by ethanol treatment in both young and aged rats. The cyclooxygenase inhibitor diclofenac, which reduces the synthesis of dilating and constricting prostanoids, enhanced the relaxation to acetylcholine in all three aged rat groups but was without significant effect in the young rats. In the presence of the nitric oxide synthase inhibitor N G-nitro-l-arginine methyl ester the relaxation to acetylcholine in control and sucrose-fed aged rats was markedly reduced compared with control rats, whereas in the young controls and in both young and aged ethanol-exposed groups, distinct relaxations to higher concentrations of acetylcholine were still present. The endothelium-independent relaxations to cromakalim, a hyperpolarizing vasodilator acting via ATP-sensitive potassium channels, were also markedly augmented by ethanol feeding in both young and aged rats. In conclusion, ethanol consumption in both young and aged rats was associated with markedly improved arterial relaxations to isoproterenol and cromakalim, as well as clearly augmented relaxation to acetylcholine during inhibition of cyclooxygenase and nitric oxide synthase. These findings suggest that especially the potassium channel-related component of arterial relaxation was augmented by long-term ethanol exposure.


2011 ◽  
Vol 300 (1) ◽  
pp. G109-G119 ◽  
Author(s):  
Martin J. J. Ronis ◽  
Leah Hennings ◽  
Ben Stewart ◽  
Alexei G. Basnakian ◽  
Eugene O. Apostolov ◽  
...  

Male Sprague-Dawley rats were chronically fed a high-unsaturated-fat diet for 130 days by using total enteral nutrition (TEN), or the same diet in which ethanol (EtOH) isocalorically replaced carbohydrate calories. Additional groups were supplemented with the antioxidant N-acetylcysteine (NAC) at 1.7 g·kg−1·day−1. Relative to an ad libitum chow-fed group, the high-fat-fed controls had three- to fourfold greater expression of fatty acid transporter CD36 mRNA and developed mild steatosis but little other hepatic pathology. NAC treatment resulted in increased somatic growth relative to controls (4.0 ± 0.1 vs. 3.1 ± 0.1 g/day) and increased hepatic steatosis score (3.5 ± 0.6 vs. 2.7 ± 1.2), associated with suppression of the triglyceride hydrolyzing protein adiponutrin, but produced no elevation in serum alanine aminotransferase (ALT). Chronic EtOH treatment increased expression of fatty acid transport protein FATP-2 mRNA twofold, resulting in marked hepatic steatosis, oxidative stress, and a twofold elevation in serum ALT. However, no changes in tumor necrosis factor-α or transforming growth factor-β expression were observed. Fibrosis, as measured by Masson's trichrome and picrosirius red staining, and a twofold increase in expression of type I and type III collagen mRNA, was only observed after EtOH treatment. Long-term EtOH treatment increased hepatocyte proliferation but did not modify the hepatic mRNAs for hedgehog pathway ligands or target genes or genes regulating epithelial-to-mesenchymal transition. Although the effects of NAC on EtOH-induced fibrosis could not be fully evaluated, NAC had additive effects on hepatocyte proliferation and prevented EtOH-induced oxidative stress and necrosis, despite a failure to reverse hepatic steatosis.


2003 ◽  
Vol 3 (2) ◽  
pp. 135-140 ◽  
Author(s):  
Rajat Sandhir ◽  
Supriya Subramanian ◽  
Ashwani Koul

2011 ◽  
Vol 23 (3) ◽  
pp. 166-172 ◽  
Author(s):  
Kemal Simsek ◽  
Hakan Ay ◽  
Turgut Topal ◽  
Mehmet Ozler ◽  
Bulent Uysal ◽  
...  

2015 ◽  
Vol 41 (10) ◽  
pp. 546-553 ◽  
Author(s):  
Keila Karine Duarte Campos ◽  
Simone Floresta Leal ◽  
Daniela Caldeira Costa ◽  
Wanderson Geraldo de Lima ◽  
Frank Silva Bezerra

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 362
Author(s):  
Malgorzata Lopatynska-Mazurek ◽  
Anna Pankowska ◽  
Ewa Gibula-Tarlowska ◽  
Radoslaw Pietura ◽  
Jolanta H. Kotlinska

The mammalian target of rapamycin (mTOR), a serine/ threonine kinase, is implicated in synaptic plasticity by controlling protein synthesis. Research suggests that ethanol exposure during pregnancy alters the mTOR signaling pathway in the fetal hippocampus. Thus, we investigated the influence of pre-treatment with rapamycin, an mTORC1 inhibitor, on the development of recognition memory deficits in adult rats that were neonatally exposed to ethanol. In the study, male and female rat pups received ethanol (5 g/kg/day) by intragastric intubation at postanatal day (PND 4-9), an equivalent to the third trimester of human pregnancy. Rapamycin (3 and 10 mg/kg) was given intraperitoneally before every ethanol administration. Short- and long-term recognition memory was assessed in the novel object recognition (NOR) task in adult (PND 59/60) rats. Locomotor activity and anxiety-like behavior were also evaluated to exclude the influence of such behavior on the outcome of the memory task. Moreover, the effects of rapamycin pre-treatment during neonatal ethanol exposure on the content of amino-acids and amines essential for the proper development of cognitive function in the dentate gyrus (DG) of the hippocampus was evaluated using proton magnetic resonance spectroscopy (1H MRS) in male adult (PND 60) rats. Our results show the deleterious effect of ethanol given to neonatal rats on long-term recognition memory in adults. The effect was more pronounced in male rather than female rats. Rapamycin reversed this ethanol-induced memory impairment and normalized the levels of amino acids and amines in the DG. This suggests the involvement of mTORC1 in the deleterious effect of ethanol on the developing brain.


Author(s):  
Augustine I. Airaodion ◽  
Emmanuel O. Ogbuagu ◽  
Ogbonnaya Ewa ◽  
Uloaku Ogbuagu ◽  
Olaide O. Awosanya ◽  
...  

Aim: This study is aimed at investigating the ameliorative efficacy of methanolic extract of Corchorus olitorius leaves against acute ethanol-induced oxidative stress in Wistar rats. Methods: Fresh plants of C. olitorius were harvested from the Institute of Agricultural Research and Training, Ibadan. The leaves were dried and extracted using soxhlet apparatus and methanol as the solvent. The methanol was evaporated in a rotary evaporator at 35°C with a yield of 2.17 g which represents a percentage yield of 8.68%. Twenty adult male Wistar rats with body weight between 120 and 150 g were used for this study. They were randomly divided into four groups of five rats each. Animals in groups 1 and 2 were administered saline solution while those in groups 3 and 4 were administered C. olitorius extract for twenty-one days. The animals were administered the extract and saline solution at a dose of 4 mL per 100 g body weight 12 hourly via oral route of administration. At the end of the treatment, they were fasted overnight and animals in groups 2 and 4 were exposed to a single dose of 70% ethanol at 12 ml/kg body weight to induce oxidative stress. After 12 hours of ethanol administration, the animals were anaesthetized using diethyl ether and were sacrificed. Liver was excised, weighed and homogenized in 50 mmol/L Tris–HCl buffer (pH 7.4) and then centrifuged at 5000 × g for 15 minutes for biochemical analysis. Supernatants were immediately kept frozen for further analysis. Results: Ethanol-induced oxidative stress significantly increased the activities of AST, ALT, LDH, LPO, CAT, SOD and GPX but decrease GSH.  These effects were regulated by C. olitorius administration. Conclusion: C. olitorius was able to remedy the effect of ethanol by regulating the oxidative stress biomarkers, thus possesses ameliorative efficacy against ethanol-induced oxidative stress and can protect the body against free radicals arising from oxidative stress.


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