Scorpion bradykinin potentiating factor mitigates lung damage induced by γ-irradiation in rats: Insights on AngII/ACE/Ang(1–7) axis

The goal of this research is to study the mitigating impact of bradykinin potentiating factor (BPF) found in scorpion Androctonus bicolor venom on irradiation-induced lung damage as a new functional target for angiotensin-converting enzyme inhibitors (ACEIs). Male rats were exposed to 7 Gy of γ-radiation as a single dose, with a biweekly intraperitoneal injection of 1 μg/g BPF. Gamma irradiation not only boosted the ACE activity and angiotensin II (Ang II) level, in lung tissue but also significantly depressed the angiotensin (1–7) (Ang (1–7)) that, lead to lung toxicity through a significant elevation of pulmonary levels of CXC-chemokine receptor 4 (CXCR4), toll-like receptor 4 (TLR4), nitric oxide (NO) and lactate dehydrogenase (LDH) activity with a marked disruption in oxidative stress markers, via a reduction in the level of total thiol (tSH) and superoxide dismutase (SOD) activity associated with an elevation in protein carbonyl (PCO) contents. In addition, apoptotic consequences of gamma irradiation were evidenced by raising the levels of mitogen-activated protein kinase (MAPK), C-Jun N-Terminal Kinases (JNK), and cleaved caspase-3. BPF administration leads to ACE inhibition, consequently sustaining decreased Ang II alongside increased Ang (1–7) production. Those sensitive molecules reduce irradiated lung issues. In conclusion, BPF significantly diminished the biochemical and histopathological consequences of radiation through renin-angiotensin system (RAS) control and ACE suppression in the lung.