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

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.

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

AJP Renal Physiology ◽

10.1152/ajprenal.00417.2014 ◽

2015 ◽

Vol 308 (7) ◽

pp. F689-F696 ◽

Cited By ~ 25

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.

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Protective Effects of Quercetin on Livers from Mice Exposed to Long-Term Cigarette Smoke

BioMed Research International ◽

10.1155/2020/2196207 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Pedro A. Machado-Junior ◽

Natália P. S. Araújo ◽

Ana B. F. Souza ◽

Thalles F. Castro ◽

Michel Oliveira ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Cigarette Smoke ◽

Liver Diseases ◽

Inflammatory Cells ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Protective Effects ◽

Histopathological Changes

Cigarette smoke is highly toxic, and it can promote increased production of reactive species and inflammatory response and leads to liver diseases. Quercetin is a flavonoid that displays antioxidant and anti-inflammatory activities in liver diseases. This study aimed at evaluating the protective effects of quercetin on livers from mice exposed to long-term cigarette smoke exposure. Male C57BL/6 mice were divided into five groups: control (CG), vehicle (VG), quercetin (QG), cigarette smoke (CSG), quercetin, and cigarette smoke (QCSG). CSG and QCSG were exposed to cigarette smoke for sixty consecutive days; at the end of the exposures, all animals were euthanized. Mice that received quercetin daily and were exposed to cigarette smoke showed a reduced influx of inflammatory cells, oxidative stress, inflammatory reaction, and histopathological changes in the liver, compared to CSG. These results suggest that quercetin may be an effective adjuvant for treating damage to the liver due to cigarette smoke exposure.

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Long-term cigarette smoke exposure inhibits histone deacetylase 2 expression and enhances the nuclear factor-κB activation in skeletal muscle of mice

Oncotarget ◽

10.18632/oncotarget.18089 ◽

2017 ◽

Vol 8 (34) ◽

pp. 56726-56736 ◽

Cited By ~ 5

Author(s):

Dongmei Huang ◽

Zhiying Ma ◽

Yili He ◽

Ying Xiao ◽

Honglin Luo ◽

...

Keyword(s):

Skeletal Muscle ◽

Histone Deacetylase ◽

Cigarette Smoke ◽

Nuclear Factor Κb ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Nuclear Factor ◽

Histone Deacetylase 2

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Passive cigarette smoke exposure inhibits ultraviolet light B-induced skin tumors in SKH-1 hairless mice by blocking the nuclear factor kappa B signalling pathway

Experimental Dermatology ◽

10.1111/j.1600-0625.2007.00685.x ◽

2008 ◽

Vol 17 (9) ◽

pp. 780-787 ◽

Cited By ~ 5

Author(s):

Koteswara R. Gottipati ◽

Henrik Poulsen ◽

Barry Starcher

Keyword(s):

Cigarette Smoke ◽

Ultraviolet Light ◽

Nuclear Factor Kappa B ◽

Smoke Exposure ◽

Skin Tumors ◽

Signalling Pathway ◽

Cigarette Smoke Exposure ◽

Nuclear Factor ◽

Hairless Mice ◽

Ultraviolet Light B

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

European Addiction Research ◽

10.1159/000518204 ◽

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

Objective: 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. Method: We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (N = 8); the electronic cigarette group (N = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (N = 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. Results: Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (p < 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 (p < 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 (p < 0.000). Conclusion: Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

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