The HIV-1 Transactivator Factor (Tat) Induces Enterocyte Apoptosis through a Redox-Mediated Mechanism
Figure 12
Schematic representation of the mechanism of HIV Tat viral protein-induced oxidative damage to the intestinal mucosa and the protective role of the antioxidant N-acetylcysteine (NAC).
Tat induces oxidative stress by increasing the ROS intracellular level and deranging the GSH/GSSG ratio. This leads to programmed cell death (apoptosis) and an increase in epithelial damage. Together with ion secretion [15] and altered glucose transport [39], these steps could represent key mechanisms in HIV enteropathy. Pretreatment with the antioxidant NAC restores the oxidative stress and cell apoptosis, thus protecting intestinal mucosa from gut dysfunction.