Oxidative damage and histopathological changes in lung of rat chronically exposed to nicotine alone or associated to ethanol

Dhouib, Hanène; Jallouli, Manel; Draief, Monia; Bouraoui, Saâdia; El-Fazaâ, Saloua

doi:10.1016/j.patbio.2015.10.001

Cited by 29 publications

(32 citation statements)

References 62 publications

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“…In fact, pulmonary histopathological alterations, such as emphysema, congestion and hemorrhage, were less marked in rats treated with both nicotine and EtOH compared to rats treated with nicotine only. In addition, occurrence of MCS-related oxidative damage to the lung was documented by increased levels of antioxidant enzyme activities (superoxide dismutase and catalase), which were less pronounced when nicotine was combined with EtOH [31]. Likewise, the highest levels of GSH were detected in the lungs of alcohol-addicted Wistar rats that were simultaneously exposed to CS and EtOH [32].…”

Section: Discussionmentioning

confidence: 99%

Modulation by Ethanol of Cigarette Smoke Clastogenicity in Cells of Adult Mice and of Transplacentally Exposed Fetuses

Balansky¹,

Maestra

Micale

et al. 2016

PLoS ONE

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Cigarette smoke (CS) and ethanol (EtOH) are known to synergize in the causation of cancers of the upper aerodigestive tract and of the liver. Little is known about possible interactions between these agents in other organs. These premises prompted us to evaluate the clastogenic effects resulting from the inhalation for 3 weeks of mainstream CS and oral administration of EtOH, which were tested either individually or in combination in cells of adult BDF1 mice and their fetuses. CS exerted clastogenic effects in haematopoietic cells of adult male mice by increasing the frequency of micronucleated erythroid cells both in bone marrow and in peripheral blood as well as the frequency of micronucleated and polynucleated pulmonary alveolar macrophages. Likewise, exposure to CS of pregnant mice resulted in a clastogenic damage in maternal bone marrow cells and in the liver and peripheral blood of their fetuses. Under all experimental conditions, EtOH was consistently devoid of clastogenic effects when given alone. In adult mice, EtOH exhibited a mild stimulating effect on the clastogenicity of CS in haematopoietic cells, while an opposite effect was observed in the respiratory tract, where EtOH attenuated the cytogenetic alterations induced by CS in pulmonary alveolar macrophages. At variance with the mild synergism observed in haematopoietic cells of adult mice, EtOH inhibited the clastogenicity of CS in the liver and peripheral blood cells of transplacentally exposed fetuses. Therefore, the effects of EtOH in CS-exposed mice show different trends depending both on the life stage and on the cells analyzed.

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Section: Discussionmentioning

confidence: 99%

Modulation by Ethanol of Cigarette Smoke Clastogenicity in Cells of Adult Mice and of Transplacentally Exposed Fetuses

Balansky¹,

Maestra

Micale

et al. 2016

PLoS ONE

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“…All the experimental drug delivery cycle is 10 days according to other studies (Dong et al, ; Hosseinzadeh, Tafaghodi, Abedzadeh, & Taghiabadi, ). The mice in control group were intragastrically administrated with normal saline (1 ml/kg/day; Dhouib, Jallouli, Draief, & Bouraoui, ) for 10 days. Mice in model group were intragastrically administrated with bromocriptine ((5'α)‐2‐Bromo‐12′‐hydroxy‐5′‐(2‐methylpropyl)‐3′,6′,18‐trioxo‐2′‐(propan‐2‐yl)ergotaman; purity>95%; 1.6 mg/kg/day; Dong et al, ) for 10 days.…”

Section: Methodsmentioning

confidence: 99%

“…The mice in control group were intragastrically administrated with normal saline (1 ml/kg/day; Dhouib, Jallouli, Draief, & Bouraoui, 2015) for 10 days. Mice in model group were intragastrically administrated with bromocriptine ((5'α)-2-Bromo-12′-hydroxy-5′-(2methylpropyl)-3′,6′,18-trioxo-2′-(propan-2-yl)ergotaman; purity>95%;…”

Section: Experimental Design and Treatmentsmentioning

confidence: 99%

Quercetin improves postpartum hypogalactia in milk‐deficient mice via stimulating prolactin production in pituitary gland

Lin

Wang²,

Yao

et al. 2018

Phytotherapy Research

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Postpartum dysgalactia is a common clinical problem for lactating women. Seeking out the safe and efficient phytoestrogens will be a promising strategy for postpartum dysgalactia therapy. In this study, the postpartum mice within four groups, including control group, the model group, and the treatment groups intragastrically administrated with normal saline, bromocriptine, bromocriptine plus 17α-ethinyl estradiol, and bromocriptine plus quercetin, respectively, were used. The results showed that quercetin, a kind of natural phytoestrogen, could efficiently promote lactation yield and mammary gland development in the agalactosis mice produced by bromocriptine administration. Mechanically, quercetin, such as 17α-ethinyl estradiol, significantly stimulated prolactin (PRL) production and deposition in the mammary gland in the agalactosis mice determined by western blotting, quantitative polymerase chain reaction, and enzyme-linked immunosorbent assay, respectively. Furthermore, quercetin could increase the expression of β-casein, stearoyl-CoA desaturase, fatty acid synthase, and α-lactalbumin in the breast tissues that are responsible for the production of fatty acid, lactose, and galactose in the milk at the transcriptional level determined by quantitative polymerase chain reaction. Specifically, quercetin promoted primary mammary epithelial cell proliferation and stimulated prolactin receptor (PRLR) expression probably via AKT activation in vitro. In conclusion, this study indicates that estrogen-like quercetin promotes mammary gland development and lactation yield in milk-deficient mice, probably via stimulating PRL expression and release from the pituitary gland, as well as induces PRLR expression in primary mammary epithelial cells.

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“…In rats, nicotine has been shown to affect the oxidative state of the lung by increasing the activity of superoxide dismutase, an important protective mechanism in lung [151,152]. Overexpression of superoxide dismutase was protective against fibrosis in the bleomycin model [153].…”

Section: Anti-oxidantsmentioning

confidence: 99%

“…Some have postulated that cigarette smoke promotes the induction of oxidant stress [146]. In rats, nicotine alone has been shown to affect the oxidative state of the lung by increasing the activity of superoxide dismutase, an important protective mechanism in lung [151,152].…”

Section: Introductionmentioning

confidence: 99%

The role of nicotine, a7 nicotinic acetylcholine receptors and extracellular matrix remodeling in pulmonary fibrosis.

Vicary¹

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Oxidative damage and histopathological changes in lung of rat chronically exposed to nicotine alone or associated to ethanol

Cited by 29 publications

References 62 publications

Modulation by Ethanol of Cigarette Smoke Clastogenicity in Cells of Adult Mice and of Transplacentally Exposed Fetuses

Modulation by Ethanol of Cigarette Smoke Clastogenicity in Cells of Adult Mice and of Transplacentally Exposed Fetuses

Quercetin improves postpartum hypogalactia in milk‐deficient mice via stimulating prolactin production in pituitary gland

The role of nicotine, a7 nicotinic acetylcholine receptors and extracellular matrix remodeling in pulmonary fibrosis.

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