Immunohistochemical analysis of bcl-2 and p53 in rabbit lung tissue following nurinol pesticide exposure

Exposure to the pesticide Nurinol, a chlorpyrifos- and cypermethrin-based formulation, can induce severe oxidative damage in lung tissue. This study examined the immunohistochemical expression of the anti-apoptotic protein Bcl-2 and the pro-apoptotic marker p53 in rabbit lungs following 30-day (acute) and 120-day (chronic) Nurinol inhalation exposure, with and without antioxidant therapy. Lung tissue sections were stained for Bcl-2 and p53, and positive cell expression was quantified. In rabbits exposed to Nurinol alone, Bcl-2 expression was markedly suppressed, while p53 levels were elevated, indicating a loss of anti-apoptotic protection and activation of apoptosis. Antioxidant co-therapy significantly preserved Bcl-2 expression and reduced p53 accumulation in lung cells, particularly in the 30-day exposure group. In the 120-day exposure groups, antioxidant treatment also mitigated the alterations in Bcl-2 and p53, though to a lesser extent than in acute exposure. These findings suggest that Nurinol-induced lung injury involves enhanced apoptosis signaling and diminished cell survival mechanisms, and that antioxidant intervention can partially counteract these pathological processes.