scholarly journals l-Carnitine reverses maternal cigarette smoke exposure-induced renal oxidative stress and mitochondrial dysfunction in mouse offspring

2015 ◽  
Vol 308 (7) ◽  
pp. F689-F696 ◽  
Author(s):  
Long T. Nguyen ◽  
Stefanie Stangenberg ◽  
Hui Chen ◽  
Ibrahim Al-Odat ◽  
Yik L. Chan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cigarette Smoke ◽  
Maternal Smoking ◽  
Smoke Exposure ◽  
Male Offspring ◽  
Antioxidant Defenses ◽  
Cigarette Smoke Exposure ◽  
Pregnancy And Lactation ◽  
Underlying Mechanisms

Maternal smoking is associated with metabolic disorders, renal underdevelopment, and a predisposition to chronic kidney disease in offspring, yet the underlying mechanisms are unclear. By exposing female Balb/c mice to cigarette smoke for 6 wk premating and during gestation and lactation, we showed that maternal smoke exposure induced glucose intolerance, renal underdevelopment, inflammation, and albuminuria in male offspring. This was associated with increased renal oxidative stress and mitochondrial dysfunction at birth and in adulthood. Importantly, we demonstrated that dietary supplementation of l-carnitine, an amino acid shown to increase antioxidant defenses and mitochondrial function in numerous diseases, in smoke-exposed mothers during pregnancy and lactation significantly reversed the detrimental maternal impacts on kidney pathology in these male offspring. It increased SOD2 and glutathione peroxidase 1, reduced ROS accumulation, and normalized levels of mitochondrial preprotein translocases of the outer membrane, and oxidative phosphorylation complexes I–V in the kidneys of mouse progeny after intrauterine cigarette smoke exposure. These findings support the hypothesis that oxidative stress and mitochondrial dysfunction are closely linked to the adverse effects of maternal smoking on male offspring renal pathology. The results of our study suggest that l-carnitine administration in cigarette smoke-exposed mothers mitigates these deleterious renal consequences.

scholarly journals Effect of long-term maternal smoking on the offspring’s lung health

2017 ◽  
Vol 313 (2) ◽  
pp. L416-L423 ◽  
Author(s):  
Surpon Sukjamnong ◽  
Yik Lung Chan ◽  
Razia Zakarya ◽  
Sonia Saad ◽  
Pawan Sharma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Maternal Smoking ◽  
Smoke Exposure ◽  
Male Offspring ◽  
Mitogen Activated Protein Kinase ◽  
Cigarette Smoke Exposure ◽  
Nuclear Factor ◽  
The Impact

Maternal smoking during pregnancy contributes to long-term health problems in offspring, especially respiratory disorders that can manifest in either childhood or adulthood. Receptors for advanced glycation end products (RAGE) are multiligand receptors abundantly localized in the lung, capable of responding to by-products of reactive oxygen species and proinflammatory responses. RAGE signaling is a key regulator of inflammation in cigarette smoking-related pulmonary diseases. However, the impact of maternal cigarette smoke exposure on lung RAGE signaling in the offspring is unclear. This study aims to investigate the effect of maternal cigarette smoke exposure (SE), as well as mitochondria-targeted antioxidant [mitoquinone mesylate (MitoQ)] treatment, during pregnancy on the RAGE-mediated signaling pathway in the lung of male offspring. Female Balb/c mice (8 wk) were divided into a sham group (exposed to air), an SE group (exposed to cigarette smoke), and an SE + MQ group (exposed to cigarette smoke with MitoQ supplement from mating). The lungs from male offspring were collected at 13 wk. RAGE and its downstream signaling, including nuclear factor-κB and mitogen-activated protein kinase family consisting of extracellular signal-regulated kinase 1, ERK2, c-JUN NH2-terminal kinase (JNK), and phosphorylated JNK, in the lung were significantly increased in the SE offspring. Mitochondrial antioxidant manganese superoxide dismutase was reduced, whereas IL-1β and oxidative stress response nuclear factor (erythroid-derived 2)-like 2 were significantly increased in the SE offspring. Maternal MitoQ treatment normalized RAGE, IL-1β, and Nrf-2 levels in the SE + MQ offspring. Maternal SE increased RAGE and its signaling elements associated with increased oxidative stress and inflammatory cytokines in offspring lungs, whereas maternal MitoQ treatment can partially normalize these changes.

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

scholarly journals Impact of maternal cigarette smoke exposure on brain inflammation and oxidative stress in male mice offspring

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yik Lung Chan ◽  
Sonia Saad ◽  
Carol Pollock ◽  
Brian Oliver ◽  
Ibrahim Al-Odat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Brain Inflammation ◽  
Cigarette Smoke Exposure ◽  
Male Mice ◽  
And Oxidative Stress

scholarly journals Impact of acute exposure to cigarette smoke on airway gene expression

2018 ◽  
Vol 50 (9) ◽  
pp. 705-713 ◽  
Author(s):  
E. Billatos ◽  
A. Faiz ◽  
Y. Gesthalter ◽  
A. LeClerc ◽  
Y. O. Alekseyev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lung Cancer ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Acute Exposure ◽  
Cigarette Smoke Exposure ◽  
Airway Epithelial ◽  
Long Term Effects ◽  
Chronic Smoking

Background: Understanding effects of acute smoke exposure (ASE) on airway epithelial gene expression and their relationship with the effects of chronic smoke exposure may provide biological insights into the development of smoking-related respiratory diseases. Methods: Bronchial airway epithelial cell brushings were collected from 63 individuals without recent cigarette smoke exposure and before and 24 h after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Results: We identified 91 genes differentially expressed 24 h after ASE (false discovery rate < 0.25). ASE induced genes involved in xenobiotic metabolism, oxidative stress, and inflammation and repressed genes related to cilium morphogenesis and cell cycle. While many genes altered by ASE are altered similarly in chronic smokers, metallothionein genes are induced by ASE and suppressed in chronic smokers. Metallothioneins are also suppressed in current and former smokers with lung cancer relative to those without lung cancer. Conclusions: Acute exposure to as little as three cigarettes and chronic smoking induce largely concordant changes in airway epithelial gene expression. Differences in short-term and long-term effects of smoking on metallothionein expression and their relationship to lung cancer requires further study given these enzymes’ role in the oxidative stress response.

scholarly journals Human SLPI inactivation after cigarette smoke exposure in a new in vivo model of pulmonary oxidative stress

2001 ◽  
Vol 281 (2) ◽  
pp. L412-L417 ◽  
Author(s):  
Eleonora Cavarra ◽  
Monica Lucattelli ◽  
Federica Gambelli ◽  
Barbara Bartalesi ◽  
Silvia Fineschi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Lavage Fluid ◽  
Antioxidant Defenses ◽  
Cigarette Smoke Exposure ◽  
In Vivo Model ◽  
Protein Thiols ◽  
Total Antioxidant ◽  
Antitrypsin Activity

The role of oxidative stress in inactivating antiproteases is the object of debate. To address this question, we developed an in vivo model of pulmonary oxidative stress induced by cigarette smoke (CS) in mice. The major mouse trypsin inhibitor contrapsin is not sensitive to oxidation, and the mouse secretory leukoprotease inhibitor (SLPI) does not inhibit trypsin. Instead, human recombinant (hr) SLPI inhibits trypsin and is sensitive to oxidation. Thus we determined the effect of CS in vivo on hrSLPI antiproteolytic function in the airways of mice. CS caused a significant decrease in total antioxidant capacity in bronchoalveolar lavage fluid (BALF) and significant changes in oxidized glutathione, ascorbic acid, protein thiols, and 8-epi-PGF2α. Intratracheal hrSLPI significantly increased BALF antitryptic activity. CS induced a 50% drop in the inhibitory activity of hrSLPI. Pretreatment with N-acetylcysteine prevented the CS-induced loss of hrSLPI activity, the decrease in antioxidant defenses, and the elevation of 8-epi-PGF-2α. Thus an inactivation of hrSLPI was demonstrated in this model. This is a novel model for studying in vivo the effects of CS oxidative stress on human protease inhibitors with antitrypsin activity.

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