Glutamine--a popular nutritional supplement, non-toxic amino acid, and an essential interorgan and intercellular ammonia transporter--can destroy the neurons' mitochondria. When glutamine enters (like a Trojan horse) into the mitochondria, in the presence of glutaminase, it reacts with water and yields glutamate and excess ammonia which opens gates in the membrane of the mitochondria and thereby destroys it. The mechanistic details underlying the molecular basis of the catabolic production of excess ammonia remain unclear. In the present paper, both 5-oxoproline-mediated and direct pathways for glutamine deamidation are studied using wave function and density functional theories. The mechanisms are studied both in the gas phase and in aqueous solution using the polarizable continuum model (PCM) and solvent model on density (SMD) solvation models. Among three glutamine deamidation pathways, a two-step pathway, GDB, shows the lowest gas phase barrier height of 189 kJ/mol with the G3MP2B3 level of theory. Incorporation of solvent through PCM and SMD models reduces the barrier height to 183 and 174 kJ/mol, respectively. For the hydrolysis of 5-oxoproline, a two-step mechanism, pathway PH-B, provides a lower gas phase energy barrier (187 kJ/mol) compared to one-step (201 kJ/mol) and three-step (227 kJ/mol) pathways at G3MP2B3. Although direct hydrolysis with OH(-), pathway DHE, has the lowest gas phase barrier of 135 kJ/mol, the solvent has little effect on the barrier. For the direct hydrolysis with OH(-)/H2O, pathway DHF, the overall barrier is 143 kJ/mol, in the gas phase at G3MP2B3. In aqueous solution, the overall barrier decreases to 76 and 75 kJ/mol with PCM and SMD, respectively, at B3LYP/6-31+G(d,p), making this the most plausible mechanism. Compared to PCM, SMD predicts lower barriers for nearly all pathways investigated.