Ethanol consumption did not alter TBARS levels in the rat CC indicating that, despite the increase in O2− generation, no alteration in lipid peroxidation was evidenced in this tissue. Moreover, ethanol intake did not alter GSH levels in the CC or plasma, indicating that the treatment did not diminished cellular and systemic non-enzymatic antioxidant capacity. On the other hand, ethanol increased SB939 TBARS concentration and did not affect plasma SOD activity. These results suggest that ethanol consumption differently modulates cellular and systemic antioxidants systems as described previously [27] and [28].
5. Conclusion
The major new finding of our study is directional selection chronic ethanol consumption induced ED and increased ET-1-induced contraction of the rat CC by a mechanism that involves decreased generation of H2O2 and vasodilator prostanoids as well as increased activation of the RhoA/Rho-kinase pathway. These results provide new insights into the mechanism underlying ethanol-induced ED.
5. Conclusion
The major new finding of our study is directional selection chronic ethanol consumption induced ED and increased ET-1-induced contraction of the rat CC by a mechanism that involves decreased generation of H2O2 and vasodilator prostanoids as well as increased activation of the RhoA/Rho-kinase pathway. These results provide new insights into the mechanism underlying ethanol-induced ED.
