DNA polymerase beta is involved in the protection against the cytotoxicity and genotoxicity of cigarette smoke

Cui, Jie; Zhao, Wei; Xu, Xin; Yang, Mo; Ren, Yaou; Zhang, Zunzhen

doi:10.1016/j.etap.2012.05.012

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…These ndings are consistent with earlier research showing that components of cigarette smoke inhibit DNA repair [33][34][35]. Among them, as oxidative stress increases, the base excision repair capacity, which plays a crucial part in preventing DNA oxidative damage from being exposed to cigarette smoke, decreases, aggravating DNA damage [37]. The preservation of cellular life activities and genomic stability may be impacted by the delayed damage repair caused by malfunctioning of these repair mechanisms [35,36].…”

Section: Discussionsupporting

confidence: 90%

Integrated mRNA- and miRNA-sequencing analyses unveil the underlying mechanism of tobacco pollutant-induced developmental toxicity in zebrafish embryos

Zhong,

Chen,

Lin

et al. 2023

Preprint

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Tobacco pollutants are prevalent in the environment, leading to inadvertent exposure of pregnant females. Although there are studies examining the toxic effects of these pollutants on the development, they are not yet able to fully elucidate the potential underlying mechanisms. Therefore, in this study, we aimed to investigate the developmental toxicity induced by cigarette smoke extract (CSE) at concentrations of 0.25%, 1%, and 2.5% using a zebrafish embryo toxicity test and integrated transcriptomic analysis of microRNA (miRNA) and messenger RNA (mRNA). The findings revealed that CSE caused developmental toxicity, including increased mortality and decreased incubation rate, in a dose-dependent manner. Moreover, CSE induced malformations and apoptosis, specifically in the head and heart of zebrafish larvae. mRNA- and miRNA-sequencing analyses were used to compare changes in the expression of genes and miRNAs in zebrafish larvae. The results of bioinformatics analysis indicate that the mechanism underlying CSE-induced developmental toxicity was associated with genetic material damage, apoptosis disorder, as well as lipid metabolism disturbance. Morever, the enrichment analysis and RT-qPCR analysis results shown ctsba gene play crucial function in embryo developmental apoptosis, whereas fads2 gene mainly regulated lipid metabolic toxicity. The results of this study improve the current understanding of CSE-induced developmental toxicity in zebrafish embryos and contribute insights for the formulation of novel preventive strategies against tobacco pollutants during early embryonic development.

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Section: Discussionsupporting

confidence: 90%

Integrated mRNA- and miRNA-sequencing analyses unveil the underlying mechanism of tobacco pollutant-induced developmental toxicity in zebrafish embryos

Zhong,

Chen,

Lin

et al. 2023

Preprint

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“…For example, oxidative stress is an important mechanism that alters the balance between proliferation and apoptosis in fibroblasts (Müller & Gebel, 1998). Genetic damage is also induced by CS extract (Cui et al, 2012). Depletion of antioxidants by several CS extract components like acrolein and aldehydes compromises the defensive mechanisms of fibroblasts and promotes cell damage (Colombo et al, 2012;Ishii et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity evaluation of electronic cigarette vapor extract on cultured mammalian fibroblasts (ClearStream-LIFE): comparison with tobacco cigarette smoke extract

Romagna¹,

Allifranchini²,

Bocchietto³

et al. 2013

Inhalation Toxicology

172

130

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“…The protective role of tobacco in preventing increased NPB, NBUDS, APOP, and NECRO frequencies in all participants was another interesting result. The genotoxic effects of tobacco smoke reported only for MN in PZOI have been described in previous studies related to oxidative stress induction and the regulation of the IL-8, IL-6, and TNF-α inflammatory cytokine pathways [ 35 ]. However, in concordance with the results obtained for NPB, NBUDS, APOP, and NECRO, other studies have suggested a protective effect of tobacco exposure via an individual adaptative response in exposed individuals.…”

Section: Discussionmentioning

confidence: 99%

Genetic Instability among Hitnü People Living in Colombian Crude-Oil Exploitation Areas

Galeano-Páez

Ricardo-Caldera

Jiménez-Vidal

et al. 2022

IJERPH

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Oil exploitation, drilling, transportation, and processing in refineries produces a complex mixture of chemical compounds, including polycyclic aromatic hydrocarbons (PAHs), which may affect the health of populations living in the zone of influence of mining activities (PZOI). Thus, to better understand the effects of oil exploitation activities on cytogenetic endpoint frequency, we conducted a biomonitoring study in the Hitnü indigenous populations from eastern Colombia by using the cytokinesis micronucleus cytome assay (CBMN-cyt). PAH exposure was also measured by determine urine 1-hydroxypyrene (1-OHP) using HPLC. We also evaluated the relationship between DNA damage and 1-OHP levels in the oil exploitation area, as well as the modulating effects of community health factors, such as Chagas infection; nutritional status; and consumption of traditional hallucinogens, tobacco, and wine from traditional palms. The frequencies of the CBMN-cyt assay parameters were comparable between PZOI and Hitnü populations outside the zone of influence of mining activities (POZOI); however, a non-significant incremental trend among individuals from the PZOI for most of the DNA damage parameters was also observed. In agreement with these observations, levels of 1-OHP were also identified as a risk factor for increased MN frequency (PR = 1.20) compared to POZOI (PR = 0.7). Proximity to oil exploitation areas also constituted a risk factor for elevated frequencies of nucleoplasmic bridges (NPBs) and APOP-type cell death. Our results suggest that genetic instability and its potential effects among Hitnü individuals from PZOI and POZOI could be modulated by the combination of multiple factors, including the levels of 1-OHP in urine, malnutrition, and some traditional consumption practices.

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DNA polymerase beta is involved in the protection against the cytotoxicity and genotoxicity of cigarette smoke

Cited by 8 publications

References 32 publications

Integrated mRNA- and miRNA-sequencing analyses unveil the underlying mechanism of tobacco pollutant-induced developmental toxicity in zebrafish embryos

Integrated mRNA- and miRNA-sequencing analyses unveil the underlying mechanism of tobacco pollutant-induced developmental toxicity in zebrafish embryos

Cytotoxicity evaluation of electronic cigarette vapor extract on cultured mammalian fibroblasts (ClearStream-LIFE): comparison with tobacco cigarette smoke extract

Genetic Instability among Hitnü People Living in Colombian Crude-Oil Exploitation Areas

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