scholarly journals Alteration of oxidative-stress and related marker levels in mouse colonic tissues and fecal microbiota structures with chronic ethanol administration: Implications for the pathogenesis of ethanol-related colorectal cancer

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246580
Author(s):  
Hideo Ohira ◽  
Atsuki Tsuruya ◽  
Daiki Oikawa ◽  
Wao Nakagawa ◽  
Rie Mamoto ◽  
...  

Chronic ethanol consumption is a risk factor for colorectal cancer, and ethanol-induced reactive oxygen species have been suggested to play important roles in the pathogenesis of ethanol-related colorectal cancer (ER-CRC). In this study, the effects of 10-week chronic administration of ethanol on the colonic levels of oxidative stress and advance glycation end product (AGE) levels, as well as fecal microbiota structures, were examined in a mouse model. Chronic oral administration of ethanol in mice (1.0 mL of 1.5% or 5.0% ethanol (v/v) per day per mouse, up to 10 weeks) resulted in the elevation of colonic levels of oxidative stress markers (such as 8-hydroxy-2’-deoxyguanosine and 4-hydroxynonenal) compared to control mice, and this was consistently accompanied by elevated levels of inflammation-associated cytokines and immune cells (Th17 and macrophages) and a decreased level of regulatory T (Treg) cells to produce colonic lesions. It also resulted in an alteration of mouse fecal microbiota structures, reminiscent of the alterations observed in human inflammatory bowel disease, and this appeared to be consistent with the proposed sustained generation of oxidative stress in the colonic environment during chronic ethanol consumption. Moreover, the first experimental evidence that chronic ethanol administration results in elevated levels of advanced glycation end products (AGEs) and their receptors (RAGE) in the colonic tissues in mice is also shown, implying enhanced RAGE-mediated signaling with chronic ethanol administration. The RAGE-mediated signaling pathway has thus far been implicated as a link between the accumulation of AGEs and the development of many types of chronic colitis and cancers. Thus, enhancement of this pathway likely exacerbates the ethanol-induced inflammatory states of colonic tissues and might at least partly contribute to the pathogenesis of ER-CRC.

Gut ◽  
1998 ◽  
Vol 42 (3) ◽  
pp. 426-430 ◽  
Author(s):  
I D Norton ◽  
M V Apte ◽  
P S Haber ◽  
G W McCaughan ◽  
R C Pirola ◽  
...  

Background—The mechanisms responsible for the initiation of alcoholic pancreatitis remain elusive. However, there is an increasing body of evidence that reactive oxygen species play a role in both acute and chronic pancreatitis. In the liver, cytochrome P4502E1 (CYP2E1, the inducible ethanol metabolising enzyme) is one of the proposed pathways by which ethanol induces oxidative stress.Aims—To determine whether CYP2E1 is present in the pancreas and, if so, whether it is inducible by chronic ethanol feeding.Methods—Eighteen male Sprague-Dawley rats were pair fed liquid diets with or without ethanol as 36% of energy for four weeks. CYP2E1 levels were determined by western blotting of microsomal protein from both pancreas and liver. Messenger RNA (mRNA) levels for CYP2E1 were quantified using dot blots of total pancreatic RNA.Results—CYP2E1 was found in the pancreas. Furthermore, the amount of CYP2E1 was greater in the pancreas of rats fed ethanol compared with controls (mean increase over controls 5.1-fold, 95% confidence intervals 2.4 to 7.7, p<0.02). In the liver, induction by ethanol of CYP2E1 was similar (mean increase over controls 7.9-fold, 95% confidence intervals 5.2 to 10.6, p<0.005). Pancreatic mRNA levels for CYP2E1 were similar in ethanol fed and control rats.Conclusions—CYP2E1 is present in the rat pancreas and is inducible by chronic ethanol administration. Induction of pancreatic CYP2E1 is not regulated at the mRNA level. The metabolism of ethanol via CYP2E1 may contribute to oxidative stress in the pancreas during chronic ethanol consumption.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Bianca Scolaro ◽  
Daniela Delwing-de Lima ◽  
José Geraldo Pereira da Cruz ◽  
Débora Delwing-Dal Magro

Objective. The aim of this study was to evaluate the influence of acute and chronic intake of mate tea on the effects elicited by acute and chronic administration of ethanol.Methods. Oxidative stress was evaluated by measuring thiobarbituric acid-reactive substances (TBARS), as well as the activities of the antioxidant enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the hippocampus and blood of rats. Male Wistar rats were randomly assigned to four groups, for both acute and chronic treatment: (1) control group, (2) treated group, (3) intoxicated group, (4) and intoxicated group treated with mate tea.Results. Both ethanol administrations significantly increased TBARS in plasma and hippocampus of rats and altered antioxidant enzyme activities, changes which were reverted by mate tea administration.Conclusions. Data indicate that acute and chronic ethanol administration induced oxidative stress in hippocampus and blood and that mate tea treatment was able to prevent this situation.


Hepatology ◽  
1999 ◽  
Vol 29 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Virginie Fataccioli ◽  
Evelyne Andraud ◽  
Monique Gentil ◽  
Samuel W. French ◽  
Helene Rouach

Redox Biology ◽  
2015 ◽  
Vol 6 ◽  
pp. 33-40 ◽  
Author(s):  
Peter S. Harris ◽  
Samantha R. Roy ◽  
Christina Coughlan ◽  
David J. Orlicky ◽  
Yongliang Liang ◽  
...  

2014 ◽  
Vol 76 ◽  
pp. S51
Author(s):  
Jaqueline Jóice Muniz ◽  
Leticia Nogueira Leite ◽  
Riccardo Lacchini ◽  
José Eduardo Tanus-Santos ◽  
Carlos Renato Tirapelli

Life Sciences ◽  
2015 ◽  
Vol 141 ◽  
pp. 44-53 ◽  
Author(s):  
Jaqueline J. Muniz ◽  
Letícia N. Leite ◽  
Bruno S. De Martinis ◽  
Fernando S. Carneiro ◽  
Carlos R. Tirapelli

2019 ◽  
Vol 97 (12) ◽  
pp. 1103-1114
Author(s):  
Gabriel T. do Vale ◽  
Arthur H. Sousa ◽  
Natália A. Gonzaga ◽  
Mariana G. de Oliveira ◽  
Alberto F.O. Justo ◽  
...  

Oxidative stress is pointed out as a major mechanism by which ethanol induces functional and structural changes in distinctive tissues. We evaluated whether ethanol consumption would increase oxidative stress and cause micturition dysfunction. Male C57BL/6J mice were treated with 20% ethanol (v/v) for 10 weeks. Our findings showed that chronic ethanol consumption reduced micturition spots and urinary volume in conscious mice, whereas in anaesthetized animals cystometric analysis revealed reduced basal pressure and increased capacity, threshold pressure, and maximum voiding. Treatment with ethanol reduced the contraction induced by carbachol in isolated bladders. Chronic ethanol consumption increased the levels of oxidant molecules and thiobarbituric acid reactive species in the mouse bladder. Upregulation of Nox2 was detected in the bladder of ethanol-treated mice. Increased activity of both superoxide dismutase and catalase were detected in the mouse bladder after treatment with ethanol. Conversely, decreased levels of reduced glutathione were detected in the bladder of ethanol-treated mice. The present study first demonstrated that chronic ethanol consumption induced micturition dysfunction and that this response was accompanied by increased levels of oxidant molecules in the mousebladder. These findings suggest that ethanol consumption is a risk factor for vesical dysfunction.


2016 ◽  
Vol 100 ◽  
pp. S151
Author(s):  
Janaina Aparecida Simplicio ◽  
Marcelo de Almeida Nakashima ◽  
Natália Almeida Gonzaga ◽  
Thiago Mattar Cunha ◽  
Carlos Renato Tirapelli

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