neurotransmitters like the opioid systems, dopamine, serotonin and gamma-amino-butyric acid (GABA) and their interactions are most affected (Chastain 2006). Being volatile, alcohol can be inhaled during ingestion and freely diffused into the airways (George, et al. 1996). This property became the basis for the breath test for estimating levels of blood alcohol (Hlastala 1998). Changes in levels of important enzymes were based on the effect of alcohol on hepatic functions and characteristics (Purohit and Brenner 2006) and other diseases (Purohit, Khalsa and Serrano, 2005). Liver damage due to alcohol has been attributed to increased oxidative stress which could be due to alterations in the liver’s antioxidant defense mechanism. Chronic ethanol intake was found to decrease cytosolic and mitochondrial glutathione/glutathione peroxidase-1 activities by 40% and 30%, respectively thereby promoting the oxidative modification of liver proteins (Bailey, et al. 2006) (Cunningham and Bailey 2001). The long-term mean daily intake of 61.6 g of ethanol increases the frequency for fatty liver and alcoholic hepatitis (Savolainen, et al. 2007).
Ethanol transfers from the blood into the air sacs in the lungs, and thus, consumption can be routinely determined by what is known as the breath test (Hlastala 1998). The breath alcohol concentration predicts the blood alcohol concentration at certain time points. The development of breath testing instruments (“breathalyzers”) has resulted in a low-cost, accurate, rapid and painless ethanol quantification. The level of alcohol exhaled is then multiplied with a factor to get an approximation of blood alcohol. However, many factors can affect the breathalyzer results; among these is diabetes (which can increase blood alcohol levels due to ketogenic reactions in the body (Berg, Tymoczko and Stryer 2002).
In emergency cases where a breath test is not suitable, ethanol concentrations can be determined from blood, urine and saliva