What primarily induces acidosis in cases of alcoholism, liver failure, and hypoxia?

In cases of alcoholism, liver failure, and hypoxia, the primary factor that induces acidosis is the depletion of cellular NAD+. In metabolic processes, especially those leading to the breakdown of alcohol (ethanol), NAD+ serves as a crucial coenzyme in various biochemical reactions, including glycolysis and the citric acid cycle. When alcohol is metabolized, it leads to an increased demand for NAD+, causing the levels to drop.

This depletion results in a shift towards anaerobic metabolism, where lactic acid begins to accumulate. The increased production of lactic acid contributes to a metabolic acidosis situation, as lactic acid dissociates to release hydrogen ions, lowering the pH of the blood and leading to acidosis.

The other choices relate to different physiological processes. Increased excretion of bicarbonate typically corresponds to mechanisms trying to compensate for acidosis, and not a direct cause. Increased retention of PCO2 is more associated with respiratory acidosis, which is not the primary mechanism in these cases. Loss of carbonic anhydrase activity would impair the bicarbonate buffering system, impacting acid-base balance, but again, it is not the primary inducer of acidosis in the context of alcoholism, liver failure, and hypoxia.

Thus