Chronic cigarette smoke exposure drives spiral ganglion neuron loss in mice

Paquette, Stephen T.; Dawes, Ryan P.; Sundar, Isaac K.; Rahman, Irfan; Brown, Edward B.; White, Patricia M.

doi:10.1038/s41598-018-24166-9

Cited by 12 publications

(11 citation statements)

References 49 publications

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“…Rosiglitazone, by induction of PPARγ and Nrf2 activity, protects against cigarette smoke-induced loss of blood-brain-barrier integrity via reduced inflammation and oxidative stress [ 160 ]. Chronic cigarette smoke exposure drives spiral ganglion neuron loss in mice [ 161 ]. The neurotoxic effects of smoking were further supported by cerebral aneurysm development and ROS formation by cigarette smoke extract and a central role of the phagocytic NADPH oxidase in this process was demonstrated by an improvement of the adverse phenotype by genetic p47phox deletion [ 162 ].…”

Section: Smoking and Neuropsychiatric Disease Riskmentioning

confidence: 99%

Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms

Hahad

Daiber

Michal

et al. 2021

IJMS

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Despite extensive efforts to combat cigarette smoking/tobacco use, it still remains a leading cause of global morbidity and mortality, killing more than eight million people each year. While tobacco smoking is a major risk factor for non-communicable diseases related to the four main groups—cardiovascular disease, cancer, chronic lung disease, and diabetes—its impact on neuropsychiatric risk is rather elusive. The aim of this review article is to emphasize the importance of smoking as a potential risk factor for neuropsychiatric disease and to identify central pathophysiological mechanisms that may contribute to this relationship. There is strong evidence from epidemiological and experimental studies indicating that smoking may increase the risk of various neuropsychiatric diseases, such as dementia/cognitive decline, schizophrenia/psychosis, depression, anxiety disorder, and suicidal behavior induced by structural and functional alterations of the central nervous system, mainly centered on inflammatory and oxidative stress pathways. From a public health perspective, preventive measures and policies designed to counteract the global epidemic of smoking should necessarily include warnings and actions that address the risk of neuropsychiatric disease.

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Section: Smoking and Neuropsychiatric Disease Riskmentioning

confidence: 99%

Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms

Hahad

Daiber

Michal

et al. 2021

IJMS

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“…Moreover, their work suggests that carbon monoxide hypoxia gives rise to free radicals in the cochlea. In mice experimentally exposed to chronic cigarette smoke, spiral ganglion neurons exhibit increased oxidative stress compared to control neurons (Paquette et al 2018). Further, nicotine administration in guinea pigs induces topographic changes to outer hair cell stereocilia (e.g., bending, disorganization, loss of stereocilia tip and side links), most markedly in the cochlear base (Abdel-Hafez et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Tobacco, but Neither Cannabis Smoking Nor Co-Drug Use, Is Associated With Hearing Loss in the National Health and Nutrition Examination Survey, 2011 to 2012 and 2015 to 2016

et al. 2022

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Introduction: A relationship between tobacco smoking and hearing loss has been reported; associations with cannabis smoking are unknown. In this cross-sectional population-based study, we examined relationships between hearing loss and smoking (tobacco, cannabis, or co-drug use). Methods: We explored the relationship between hearing loss and smoking among 2705 participants [mean age = 39.41 (SE: 0.36) years] in the National Health and Nutrition Examination Survey (2011 to 12; 2015 to 16). Smoking status was obtained via questionnaire; four mutually exclusive groups were defined: nonsmokers, current regular cannabis smokers, current regular tobacco smokers, and co-drug users. Hearing sensitivity (0.5 to 8 kHz) was assessed, and two puretone averages (PTAs) computed: low- (PTA0.5,1,2) and high-frequency (PTA3,4,6,8). We defined hearing loss as threshold >15 dB HL. Multivariable logistic regression was used to examine sex-specific associations between smoking and hearing loss in the poorer ear (selected based on PTA0.5,1,2) adjusting for age, sex, race/ethnicity, hypertension, diabetes, education, and noise exposure with sample weights applied. Results: In the age-sex adjusted model, tobacco smokers had increased odds of low- and high-frequency hearing loss compared with non-smokers [odds ratio (OR) = 1.58, 95% confidence ratio (CI): 1.05 to 2.37 and OR = 1.97, 95% CI: 1.58 to 2.45, respectively]. Co-drug users also had greater odds of low- and high-frequency hearing loss [OR = 2.07, 95% CI: 1.10 to 3.91 and OR = 2.24, 95% CI: 1.27 to 3.96, respectively]. In the fully adjusted multivariable model, compared with non-smokers, tobacco smokers had greater odds of high-frequency hearing loss [multivariable adjusted odds ratio = 1.64, 95% CI: 1.28-2.09]. However, in the fully adjusted model, there were no statistically significant relationships between hearing loss (PTA0.5,1,2 or PTA3,4,6,8) and cannabis smoking or co-drug use. Discussion: Cannabis smoking without concomitant tobacco consumption is not associated with hearing loss. However, sole use of cannabis was relatively rare and the prevalence of hearing loss in this population was low, limiting generalizability of the results. This study suggests that tobacco smoking may be a risk factor for hearing loss but does not support an association between hearing loss and cannabis smoking. More definitive evidence could be derived using physiological measures of auditory function in smokers and from longitudinal studies.

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“…It probably inhibits the Fenton reaction by binding excess iron in the environment at low doses. On the other hand, it may also reduce the formation of superoxide anions by binding NADH and disrupting the mitochondrial electrotransfer chain (22,23).…”

Section: Discussionmentioning

confidence: 99%

“…The half-life of cotinine is longer than nicotine and its residence time in the bloodstream is 48-96 hours. Since blood cotinine level is proportional to exposure to cigarette, cotinine levels are evaluated as an indicator of nicotine exposure (10,23).…”

Section: E a R L Y A C C E S Smentioning

confidence: 99%

Cotinine Effects on Peripheral Nerve Injuries: An Experimental Study

Akdağ

Dalgıç²,

Take

et al. 2021

Düzce Tıp Fakültesi Dergisi

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Aim: Cigarette smoking is a common addictive manner and one of the greatest threats to health. Nicotine is one of the main components of cigarette. The aim of this study was to reveal the effect of cotinine which is an active metabolite of nicotine, on peripheral nerve injury in rats. Material and Methods: We studied 42 male adult albino-Wistar rats that were divided into three groups with simple randomization method. Group 1 were given Cotinine® (C-5923sigma) intraperitoneally, at a dose of 0.3 mg/kg/day for 21 days. Group 2 were given ethyl alcohol, the solvent of Cotinine in the same way, dose and period. Group 3 were subjected to sciatic nerve compression injury by a clip, which has a closing pressure of 50 gr/cm 2 . Group 1 and 2 were subjected to the same type of injury at the end of 21 days. Four weeks later after trauma, both three groups were sacrificed and injured sciatic nerve sections are taken for histopathological analysis. Results: It was observed that cotinine aggravated the traumatic degeneration and as privileged caused to fibrosis. In the Schwann cells of thick-myelinated fibers exhibited higher grades of degeneration and mitochondrial augmentation. According to the multiple comparison results, the number of Wallerian degenerations in the trauma group was significantly lower than in both the drug-control (p=0.016) and drug (p<0.001) groups. This situation was estimated as a response to oxidative stress. Conclusion:This study reveals that peripheral nerve regeneration after traumatic injury may be affected negatively in smokers.

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Chronic cigarette smoke exposure drives spiral ganglion neuron loss in mice

Cited by 12 publications

References 49 publications

Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms

Smoking and Neuropsychiatric Disease—Associations and Underlying Mechanisms

Tobacco, but Neither Cannabis Smoking Nor Co-Drug Use, Is Associated With Hearing Loss in the National Health and Nutrition Examination Survey, 2011 to 2012 and 2015 to 2016

Cotinine Effects on Peripheral Nerve Injuries: An Experimental Study

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