Effects of acute alcohol consumption and vitamin E co-treatment on oxidative stress parameters in rats tongue

Abstract

The aim of this study was to evaluate the effects of acute alcohol consumption and vitamin E co-treatment upon oxidative stress parameters in rats tongue. Thirty-eight, Wistar rats were separated into five groups (alcohol, alcohol/vitamin E, control, Tween, vitamin E). Alcohol and alcohol vitamin E groups had the standard diet, and 40% alcohol on drinking water. Other groups were fed with the same standard diet and water ad libitum. Vitamin E was given by gavage to vitamin E and alcohol/vitamin E rats twice a week. Alcohol and control groups were subjected to saline gavage and Tween group to 5% Tween 80 solution, the vitamin E vehicle. At day 14, the animals were anesthetized and specimens were obtained from tongue. Lipid peroxidation (TBARS), protein oxidative damage, catalase (CAT) and superoxide dismutase (SOD) activities were quantified. Alcohol group decreased TBARS in relation to control group and alcohol vitamin-treated animals decreased TBARS when compared to Tween and vitamin E groups. SOD activity was lower and CAT activity was higher in animals treated with both alcohol and vitamin E. These results suggest that short-term alcohol consumption decreases lipid peroxidation levels. Alternatively, alcohol/vitamin E group increased CAT, showing the toxicity of this association.

The effect of ethanol on rat tongue and the possible protective role of royal jelly: Light and scanning electron microscopic study

“…Carrard et al [35] suggested that short-term alcohol consuming modifies the cellular lipid metabolism. Long period of alcohol administration should be achieved in order to determine the chronic effects on rat tongue mucosa.…”

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

“…Short-term exposure to alcohol induces changes in the redox balance (Carrard et al, 2009) and an increase in cell proliferation appears later, possibly as a consequence of longer periods of biochemical imbalance. Based on the data obtained in the present study, we suggest the involvement of hydrogen peroxide on cell proliferation, but not in relation to the increase in alcohol-related epithelial proliferation.…”

“…This phenomenon could be one of the mechanisms associated with the alcohol-mediated increase in cell proliferation rates (Valentine et al, 1985;Maito et al, 2003;Carrard et al, 2004) as well as the risk of oral cancer attributed to alcohol (Guyton & Kensler, 1993;Klaunig & Kamendulis, 2004). A previous study (Carrard et al, 2009) suggested that even a short term exposure to alcohol induced biochemical disturbances in oral mucosa of rats. In addition, Nrf2, a redox-sensitive transcription factor involved in antioxidant defenses which is usually associated to the response to xenobiotics (Motohashi & Yamamoto, 2004), could be involved in the pathogenesis of alcohol-induced cell and tissue damage.…”

“…These changes in oxidative parameters may be potentially harmful because basal levels of ROS are required for proper cell signaling (Kamata & Hirata, 1999;Genestra, 2007). A previous study (Carrard et al, 2009) demonstrated that a short-term exposure to alcohol (14 days) is capable of reducing the levels of TBARS levels in oral mucosa tissues (Carrard et al, 2009). In contrast, tissues from liver (Eke et al, 1996), testes (Nordmann et al, 1990), kidney (Pari & Suresh, 2008) and central nervous system (Emre et al, 2007) have been reported to have an increase in lipid peroxidation levels after the treatment with alcohol.…”

Effect of different presentations of resveratrol on cell proliferation and epitelial thickness of the oral mucosa of wistar rats

“…The results of these studies indicated that intermediate layer cells are responsible for increased cell proliferation, and no change was observed in basal layer cells in any group since these cells are constantly undergoing physiological division. Therefore, when there is a greater demand for cell replacement, intermediate layer cells, which normally do not proliferate very actively, show increased proliferative activity [19][20][21][22] .…”