Evaluation of the effects of Tempol on oxidative stress and angiotensin-II induced hypertension in mice exposed to nicotine from electronic and tobacco cigarettes

Abstract

Electronic cigarette (E-Cig) is commonly used as an alternative to tobacco cigarette (T-Cig), as it lacks many of the toxicants present in T-Cigs. However, the toxicological mechanisms underlying E-Cig-induced hypertension are not yet well understood. The goal of this research was to explore the effects of Tempol in reducing hypertension caused by T-Cig and E-Cig exposure by mitigating oxidative stress and regulating angiotensin-II production in mouse models subjected to T-Cig and E-Cig smoke. Male C57BL/6 J mice were assigned to eight distinct groups: Air, Air + Tempol, T-Cig, T-Cig + Tempol, NIC-free E-Cig, NIC-free E-Cig + Tempol, E-Cig, and E-Cig + Tempol. Mice exposed to smoking for 12 min per hour, 6 cycles/day, 7 days/week for 4 weeks. Blood pressure was monitored, and Angiotensin-II and cGMP levels were measured using ELISA. Oxidative stress markers (GPx, GSTA1, SOD, MDA, nitrite) were assessed by RT-PCR and biochemical assays. The collected data showed a weight loss with high blood pressure and vasoconstriction in the T-Cig and E-Cig groups. Results showed an induction of angiotensin-II, GPx, GSTA1, SOD, and MDA. In contrast, cGMP and nitrite levels were reduced in the T-Cig and E-Cig groups. Tempol treatment regulated oxidative stress markers, angiotensin-II and cGMP levels, leading to a significant reduction in blood pressure. The results indicate that Tempol is essential in reducing oxidative stress and the effects of angiotensin-II caused by T-Cig and E-Cig exposure, thereby contributing to the regulation of systemic hemodynamic function.