Pulmonary infections involving Pseudomonas aeruginosa (PA) are a complication faced by cystic fibrosis (CF) patients. The bacteria can turn into a mucoid called mucA22 by mutation of the mucA gene, which decreases the effectiveness of antibiotics. Acidified nitrite (NaNO2) was shown to be an antibacterial agent against mucA22. Previously, it was shown that the mucA22 galU double mutant had increased susceptibility to acidified nitrite treatment. The complements of this mutant bacteria were investigated to assure that there were no downstream effects after the genetic modification of the bacteria. This experiment used PA01, mucA22, mucA22 galU, and their complements in conditions mimicking those of CF patients. The hypothesis was that the genetic modification galU of PA and mucA22 should be the only mutation that affects the level of protection against acidified nitrite toxicity and not any other genes downstream of these bacteria. Bacterial cultures, incubated for 24 hours, were used to perform ten-fold serial dilutions. They were spotted onto lysogeny broth agar pH 6.5 containing nitrate as a control or nitrate plus nitrite as an experimental plate. Plates were incubated in either anaerobic (15 mM nitrite) or aerobic (30 mM nitrite) conditions. Results were recorded and then reported in CFUs/mL. The results through p-value were statistically significant and demonstrated that the galU complements were complementable. Therefore, galU is one of the genes that is involved in the protection of PA from nitrite treatment. This could lead to a potential therapeutic in the future to help ease the problems of CF patients.