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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Chronic ethanol consumption induces micturition dysfunction and alters the oxidative state of the urinary bladder

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Author(s):
do Vale, Gabriel T. [1, 2] ; Sousa, Arthur H. [1] ; Gonzaga, Natalia A. [1, 2] ; de Oliveira, Mariana G. [3] ; Justo, Alberto F. O. [3] ; Alexandre, Eduardo C. [3] ; Tanus-Santos, Jose E. [2] ; Antunes, Edson [3] ; Tirapelli, Carlos R. [4]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, DEPCH, Lab Farmacol, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Fac Med, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
[3] Univ Estadual Campinas UNICAMP, Fac Ciencias Med, Dept Farmacol, Campinas, SP - Brazil
[4] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, DEPCH, Escola Enfermagem Ribeirao Preto, DFQ, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Canadian Journal of Physiology and Pharmacology; v. 97, n. 12, p. 1103-1114, DEC 2019.
Web of Science Citations: 0
Abstract

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. (AU)

FAPESP's process: 17/24123-5 - Impact of chronic ethanol consumption in the cardiac and vascular damages induced by experimental sepsis: evaluation of the role of iNOS
Grantee:Carlos Renato Tirapelli
Support Opportunities: Regular Research Grants