The combined administration of alcohol and taurine induces mitochondrial dysfunction at the beginning of alcohol hangover in mouse brain cortex.

CUTRERA RA; KARADAYIAN AG ; CARBONE S.; CARBONE S.; LORES-ARNAIZ, SILVIA; CZERNICZYNIEC A,; LORES-ARNAIZ, SILVIA; CZERNICZYNIEC A,; CUTRERA RA; KARADAYIAN AG

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencia; 2017

SAIC-SAFIS-

The combination of alcohol intake and energy drinks is often used as a possible attenuator for hangover symptoms. Alcohol hangover (AH) is the transient state that occurs after an acute ethanol consumption episode and begins when blood alcohol concentration is zero (Weise et al., 2000). Particularly, taurine is one of the major components of energy drinks. Taurine presents physiological actions which include bile acid conjugation, detoxification, membrane stabilization, osmoregulation, neurotransmission and modulation of cellular calcium levels (Schaffer et al. 2000). Furthermore, taurine plays an important role in modulating glutamate and GABA neurotransmission (El Idrissi and Trenkner 2004). In parallel, taurine acts as an indirect antioxidant by the induction of enzymatic and non-enzymatic antioxidants (Roy and Sill 2012). Therefore, the aim of this work was to evaluate brain cortex mitochondrial function after the combined administration of taurine and alcohol in mice. Swiss male mice were divided into four experimental groups: control (saline i.p.), taurine (70 mg/kg i.p.), alcohol (3.8 g/kg i.p.) and taurine-alcohol. Mitochondria were isolated by differential centrifugation (Lores Arnaiz et al., 2004). The following parameters were evaluated at AH onset. Oxygen consumption was measured with a high-resolution oxygraph using succinate as substrate (Estabrook, 1967).Hydrogen peroxide generation rate was determined by HRP fluorometric method (Boveris, 1984). Mitochondrial membrane potential was measured by flow cytomety using TMRE probe (Bustamante et al., 2004). Results show that taurine partially prevented mitochondrial respiratory dysfunction induced by alcohol hangover, restoring state 3 and respiratory control values and maintaining mitochondrial membrane potential. Surprisingly, taurine alone induced a significant mitochondrial membrane depolarization, as compared with control values.The protective effect of taurine over oxygen consumption alterations due to hangover were not reflected in a decrease in mitochondrial generation of H2O2; in fact, taurine alone significantly increased H2O2 production rate, thus showing a controversial observation which need further studies.