Nose-Only Water-Pipe Smoke Exposure in Mice Elicits Renal Histopathological Alterations, Inflammation, Oxidative Stress, DNA Damage, and Apoptosis

Abstract

The prevalence of water-pipe tobacco smoking is increasing worldwide, and is relatively high among youth and young adults. Exposure to water-pipe smoke (WPS) has been reported to affect various systems including the respiratory, cardiovascular and reproductive systems. However, the impact of WPS exposure on the kidney has received only scant attention. Here, we assessed the effect of nose-only WPS exposure for one or four consecutive weeks on renal histology, inflammation, oxidative stress, DNA damage, and apoptosis. The duration of the session was 30 min/day and 5 days/week. Control mice were exposed to air. Light and electron microcopy analysis revealed that the WPS exposure (especially at 4-week time point) caused degeneration of the endothelial cells of the glomerular capillaries and vacuolar degenerations of the proximal convoluted tubules. WPS exposure also significantly decreased the creatinine clearance, and significantly increased proteinuria and urinary kidney injury molecule-1 (KIM-1) concentration. Kidney lipid peroxidation, reactive oxygen species, and oxidized glutathione were significantly increased. WPS exposure also affected the concentration of reduced glutathione and the activity of catalase. Likewise, renal concentrations of interleukin (IL)-6, IL-1β and KIM-1 were augmented by WPS exposure. Moreover, WPS caused DNA damage as evaluated by comet assay, and increased the expression of cleaved caspase-3 and cytochrome C in the kidney. We conclude that exposure of mice to WPS caused renal histopathological alterations, inflammation, oxidative stress, DNA damage, and apoptosis. If the latter findings could be substantiated by controlled human studies, it would be an additional cause for disquiet about an established public health concern.

The Influence of Various Smoking Categories on The Risk of Gestational Hypertension and Pre-Eclampsia

“…There are some mechanisms that may explain the increased risk of GH and PE in smokers [29]. Generally, pathomechanisms triggered by smoking (by the components of tobacco smoke) may affect the processes connected with the development of the placenta and cause damage to the structure and function of the vascular endothelium of the mother.…”

“…Generally, pathomechanisms triggered by smoking (by the components of tobacco smoke) may affect the processes connected with the development of the placenta and cause damage to the structure and function of the vascular endothelium of the mother. It was shown that exposure to tobacco smoke triggers inflammation and oxidative stress in various organs and causes impairment of thrombotic events [ 17 , 29 , 30 ]. First, it has been previously shown that lower levels of micronutrients with antioxidant properties (e.g., selenium) may increase the risk of PIH [ 8 , 9 , 31 , 32 ].…”

Ameliorative effects of curcumin and caffeic acid against short term exposure of waterpipe tobacco smoking on lung, heart and kidney in mice

“…The impact of WPS in lung tissue of rat showed many morphological changes including induce the bleeding of red blood cell, thickening of alveolar walls, Furthermore, the inflammatory cells were increased [ 29 ]. In addition, short term exposure of WPS could induce vacuolization with mild glomerular degeneration, mild degeneration of endothelial cells of glomerulus capillaries, and mild ultrastructural changes in proximal convoluted tubules in mice kidney without significant increase in amount of creatinine clearance and proteins in urine [ 32 ]. Also, WPS showed histopathological alternations and ultrastructural changes in cardiomyocyte organelles in rat ventricular tissue [ 33 ].…”

Differences in oxidative stress profile in adolescents smoking waterpipe versus cigarettes: The Irbid TRY Project

“…In animal models, exposure to Wp smoke has been shown to cause oxidative damage and subsequent tissue injury to various body organs including the lungs (Khabour et al, 2018;Khan, Sundar, & Rahman, 2018;Nemmar, Al-Salam, Beegam, Yuvaraju, & Ali, 2020a), heart (Al-Sawalha, Al-Filali, Nemmar et al, 2020b), brain (Alqudah, Alzoubi, Ma'Abrih, & Khabour, 2018;Alzoubi, Halboup, Alomari, & Khabour, 2019a, kidney (Al-Sawalha, Alsari, Khabour, & Alzoubi, 2019c;Nemmar et al, 2020c;Rababa'h, Sultan, Alzoubi, Khabour, & Ababneh, 2016), liver (Charab, Abouzeinab, & Moustafa, 2016), and reproductive organs (Ali, 2017;Al-Sawalha, Almahmmod, Alzoubi, Khabour, & Alyacoub, 2019b). These alterations include induction of oxygen-reactive species, lipid peroxidation, and alteration of antioxidative enzyme activities (Badran & Laher, 2020).…”