Mechanistic studies on the adverse cardiovascular and cerebral effects of lifestyle and environmental risk factors - e-cigarette vapour, shisha smoke and aircraft noise - in cellular and murine models
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Abstract
With improvements in hygiene and medical care, environmental risk factors like aircraft noise and lifestyle choices such as e-cigarettes and shisha smoking gained prominence in global disease burden. This study used an established mouse model to investigate the link between the neuronal and cardiovascular systems under noise exposure. After exposing mice to aircraft noise for either 4 or 28 days, blood pressure and several oxidative stress markers were elevated and endothelial function was impaired. Neuroactive and antihypertensive drugs alleviated these effects, underscoring the role of psychological stress in noise-induced cardiovascular damage. Behavioural tests post-exposure showed that while 4 days of noise did not affect behaviour, 28 days-noise exposure impaired working memory and social interaction, though not consistent with the expected anxiety-like behaviour. After my group previously demonstrated effects of vaping on the cardiovascular oxidative stress, I exposed cultured endothelial cells and macrophages to either e-cigarette vapour condensate or acrolein, to explore the source of e-cigarette-induced oxidative stress. The results showed that both exposures followed the concentration-dependent effects on both cell types, and that acrolein can promote the NADPH-oxidase activation and generation of superoxide, as already published for e-cigarette vapour. The activation of Nrf2-dependent-stress-genes was also shown in DLD1-HO1-promotor cells after exposure to e-cigarette vapour and acrolein. Additionally, we established a mouse model of shisha smoke exposure and tested the effects shisha smoking has on cardiovascular and neuronal function in mice. Endothelial function was impaired in mice exposed to shisha smoke, but interestingly, blood pressure increased only marginally, probably due to the vasodilatory effects of CO in the shisha smoke. Selected markers of oxidative stress and inflammation were elevated in the heart, aortic and lung tissue, whereas only reactive oxygen species formation was elevated in the cortex. Increased oxidative stress markers, such as NQO-1 and HO-1 point to the activation of the Nrf2-pathway as a potent antioxidant response mechanism. This activation was confirmed in the DLD1-HO1-promotor cells exposed to particulate matter as it can be produced by coal and tobacco burning during a shisha session. This work is of interest for both basic scientists and medical professionals, as it provides a deeper insight into the possible mechanisms by which environmental and lifestyle risk factors affect the cardiovascular system.