Oxidative stress and genotoxicity in Rhinella arenarum (Anura: Bufonidae) tadpoles after acute exposure to Ni-Al nanoceramics

Our goals were to determine whether acute exposure to nicotine alters neuronal nitric oxide synthase (nNOS)-dependent reactivity of cerebral arterioles and to identify a potential role for oxidative stress in nicotine-induced impairment in nNOS-dependent responses of cerebral arterioles. We measured in vivo diameter of cerebral arterioles to nNOS-dependent ( N-methyl-d-aspartate and kainate) and -independent (nitroglycerin) agonists before and during acute treatment with nicotine. We found that nNOS-dependent, but not -independent, vasodilatation was impaired during treatment with nicotine. In addition, treatment of the cerebral microcirculation with tempol (1 h before infusion of nicotine) prevented nicotine-induced impairment in nNOS-dependent vasodilatation. Furthermore, the production of superoxide anion (lucigenin chemiluminescence) was increased in parietal cortex tissue of rats by treatment with nicotine, and this increase in superoxide anion production could be inhibited by tempol. Our findings suggest that acute exposure to nicotine impairs nNOS-dependent dilatation of cerebral arterioles by a mechanism that appears to be related to the formation of superoxide anion.

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Impact of an acute exposure to ethanol on the oxidative stress status in the hippocampus of prenatal restraint stress adolescent male rats

Brain Research ◽

10.1016/j.brainres.2007.11.031 ◽

2008 ◽

Vol 1191 ◽

pp. 55-62 ◽

Cited By ~ 20

Author(s):

Mihaela Enache ◽

Vincent Van Waes ◽

Elisabeth Vinner ◽

Michel Lhermitte ◽

Stefania Maccari ◽

...

Keyword(s):

Oxidative Stress ◽

Restraint Stress ◽

Acute Exposure ◽

Male Rats ◽

Adolescent Male ◽

Oxidative Stress Status ◽

Prenatal Restraint Stress

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Acute exposure to chlorpyrifos caused NADPH oxidase mediated oxidative stress and neurotoxicity in a striatal cell model of Huntington’s disease

NeuroToxicology ◽

10.1016/j.neuro.2017.03.004 ◽

2017 ◽

Vol 60 ◽

pp. 54-69 ◽

Cited By ~ 8

Author(s):

Gifty A. Dominah ◽

Rachael A. McMinimy ◽

Sallay Kallon ◽

Gunnar F. Kwakye

Keyword(s):

Oxidative Stress ◽

Nadph Oxidase ◽

Huntington's Disease ◽

Huntington’S Disease ◽

Cell Model ◽

Acute Exposure

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Impact of acute exposure to cigarette smoke on airway gene expression

Physiological Genomics ◽

10.1152/physiolgenomics.00092.2017 ◽

2018 ◽

Vol 50 (9) ◽

pp. 705-713 ◽

Cited By ~ 11

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.

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