Perception and the influence of information toward e-cigarette smoking behavior.

INTRODUCTION: Perceptions, personal perspectives, and public awareness of e-cigarette information have a significant impact on e-cigarette smoking behavior, and provide comprehensive information that can help reduce interest in e-cigarette smoking and reduce the number of new smokers. This study aimed to investigate the perceptions towards e-cigarettes related to e-cigarette use and how that information related to people's use of them. METHODS: The data for this cross-sectional study were collected via an online questionnaire. Thai nationals who were aged ≥18 years provided data between June 2021 and January 2022. Multivariable logistic regression and the chi-squared test were used to analyze the data. RESULTS: There were 340 respondents, 76 e-cigarette users, and 264 non-e-cigarette users. Most of the perceptions of information that differed statistically significantly between e-cigarette users and non-e-cigarette users included information on regulations, products, health effects, and the effectiveness of smoking cessation. The association between factors and e-cigarette smoking behavior revealed that the perception of the product information and male gender were associated with e-cigarette smoking behavior (AOR=13.59; 95% CI: 2.35-78.60, and AOR=5.19; 95% CI: 2.87-9.40, respectively). CONCLUSIONS: The perception of e-cigarette product information and male gender were associated with e-cigarette smoking behavior.

Synergistic Effect between Eugenol and 1,8-Cineole on Anesthesia in Guppy Fish (Poecilia reticulata).

This study aimed to evaluate the synergistic effect between eugenol and 1,8-cineole on anesthesia in female guppy fish (Poecilia reticulata). Experiment I evaluated the concentrations of 0, 12.5, 25, 50, and 75 mg/L of eugenol and 0, 100, 200, 300, and 400 mg/L of 1,8-cineole for times of induction and recovery from anesthesia. Experiment II divided fish into 16 study groups, combining eugenol and 1,8-cineole in pairs at varying concentrations, based on the dosage of the chemicals in experiment I. The results of the anesthesia showed that eugenol induced fish anesthesia at concentrations of 50 and 70 mg/L, with durations of 256.5 and 171.5 s, respectively. In contrast, 1,8-cineole did not induce fish anesthesia. In combination, using eugenol at 12.5 mg/L along with 1,8-cineole at 400 mg/L resulted in fish anesthesia at a time of 224.5 s. Increasing the eugenol concentration to 25 mg/L, combined with 1,8-cineole at 300 and 400 mg/L, induced fish anesthesia at times of 259.0 and 230.5 s, respectively. For treatments with eugenol at 50 mg/L combined with 1,8-cineole at 100 to 400 mg/L, fish exhibited anesthesia at times of 189.5, 181.5, 166.0, and 157.5 s. In the case of eugenol at 75 mg/L, fish showed anesthesia at times of 175.5, 156.5, 140.5, and 121.5 s, respectively. The testing results revealed that 1,8-cineole as a single treatment could not induce fish anesthesia. However, when supplementing 1,8-cineole in formulations containing eugenol, fish exhibited a significantly faster induction of anesthesia (p < 0.05). Furthermore, all fish that underwent anesthesia were able to fully recover without any mortality. However, the shorter anesthesia duration resulted in a significantly prolonged recovery time. In conclusion, eugenol and 1,8-cineole work better together as anesthetics than when used separately, and demonstrated the safety of using these anesthetic agents on guppy fish.

Predicting mortality in paraquat poisoning through clinical findings, with a focus on pulmonary and cardiovascular system disorders.

BACKGROUND: Paraquat, one of the most widely used herbicides, poses a significant risk of mortality through self-poisoning and subsequent multiple organ failure. The primary objective aimed to identify the factors associated with death in patients poisoned by paraquat. METHODS: A cross-sectional retrospective review was conducted at a tertiary referral hospital over five years. Eligible patients presented with acute paraquat toxicity between 1 January 2016 and 31 December 2020. Medical records of 148 patients were reviewed. RESULTS: The in-hospital fatality rate was found to be 21.8%. Multivariate analysis revealed that the amount of paraquat ingested and clinical presentations, particularly pulmonary and cardiovascular system disorders, were significantly associated with mortality. CONCLUSION: Our study highlights that the amount of paraquat ingested, along with the presence of pulmonary and cardiovascular system disorders, can serve as prognostic indicators for mortality rates in cases of paraquat poisoning. These findings have important implications for physicians in predicting the prognosis and mortality of paraquat poisoning patients.

Effects of glyphosate-based herbicides and glyphosate exposure on sex hormones and the reproductive system: From epidemiological evidence to mechanistic insights.

Glyphosate-based herbicides (GBHs) containing glyphosate as the active component are extensively used worldwide. Concerns have arisen about their potential risk to human, as glyphosate has been detected in human body fluids. Current controversies surround the endocrine-disrupting properties and transgenerational inheritance of diseases and germline epimutations resulting from exposure to GBHs and glyphosate. This review discusses evidence from in vitro, in vivo, and clinical studies on their impact on sex hormone regulation and reproductive system. Evidence suggests that they act as endocrine-disrupting chemicals, which altering sex hormone levels. Mechanistically, they interfere with hormone signaling pathways by disrupting proteins involved in hormone transport and metabolism. Pathological changes have been observed in male and female reproductive systems, potentially leading to reproductive toxicity. Prenatal exposure may lead to transgenerational inheritance of pathologies and sperm epimutations. However, due to the complexity of glyphosate formulations containing adjuvants identifying higher risk components in environmental exposure becomes challenging.

Andrographolide, an Antioxidant, Counteracts Paraquat- Induced Mutagenesis in Mammalian Cells.

Paraquat (1,1'-dimethyl, 4,4'-bipyridinium dichloride; PQ), a commonly used herbicide worldwide, is both toxic and mutagenic. The mutagenic effect of PQ stems from its ability to redox-cycle, generating oxidative stress and subsequently oxidative DNA damage, which miscodes when replication is attempted. Andrographolide (AP1), the major constituent in the leaves of the herbaceous plant Andrographis paniculata, is a diterpenoid with reported antioxidant activity. The present study employed the mammalian cell line AS52 to investigate the protective effect of AP1 against PQ-induced mutagenesis. AP1 induced cytotoxicity in AS52 cells in a dose-dependent manner (IC50 = 15.7 µM), which allowed the selection of a non-lethal dose for the mutagenesis studies. While PQ was mutagenic in AS52 cells as evidenced by the increased levels of 6-TGr mutants, AP1 by itself did not increase the mutation frequency. However, co-treatment with AP1 (1-5 µM) or the antioxidant N-acetylcysteine (2 mM) almost completely counteracted the mutagenicity of PQ (10-100 µM) in AS52 cells. Taken together, these findings suggest that AP1, and likely by extension, A. paniculata extracts, are effective antioxidants that can protect against PQ-induced mutations, and thus could be a promising alternative treatment for PQ poisoning.

An engineered cell line lacking OGG1 and MUTYH glycosylases implicates the accumulation of genomic 8-oxoguanine as the basis for paraquat mutagenicity.

Paraquat (1,1'-dimethyl, 4,4'-bipyridinium dichloride; PQ), a widely used herbicide, is toxic to mammals through ingestion, inhalation and skin contact. Epidemiological data suggest that PQ is also mutagenic and carcinogenic, especially in high doses. The toxic and mutagenic properties of PQ are attributed to the ability of the molecule to redox-cycle, which generates reactive oxygen species (ROS) and subsequent oxidative stress. ROS also cause oxidative DNA damage such as 8-oxoguanine (8OG), a mutagenic base that, when replicated, causes G to T transversion mutations. The present study employed the CHO-derived cell line AS52 to quantify the mutagenic properties of low doses of PQ. By containing a functional, chromosomally-integrated copy of the bacterial gpt gene, AS52 cells a facile system for evaluating the mutagenic properties of genotoxicants. To bolster the sensitivity of this system for detecting mutagenesis of weak mutagens like PQ, and to provide a tool for mechanistic evaluation of the mutagenic process, we constructed a new AS52-derived cell line defective for 8OG DNA repair. Specifically, we employed CRISPR-Cas9 technology to knock out 8-oxoguanine DNA glycosylase (OGG1) and MUTYH glycosylase, two key enzymes involved in the base excision repair of 8OG. The double knock-out (DKO) AS52 cells were found to be more sensitive to PQ toxicity than the parental (WT) AS52 cell line. They experienced higher levels of ROS, which translated into more DNA double-strand breaks, which explained the PQ toxicity. The increased ROS levels also led to more 8OG genomic accumulation, and a higher level of mutations in the DKO cells, suggesting that PQ mutagenesis is mediated primarily by 8OG genomic accumulation. Consistent with this view, antioxidant co-treatment lowered induced cellular ROS and PQ-induced mutagenesis. Taken together, our data demonstrate the strong protective role of OGG1 and MUTYH against PQ-induced mutagenesis. Moreover, our experiments establish the engineered OGG1-/-MUTYH-/- AS52 cell line and associated methods as a versatile cellular system for studying in quantitative terms the mutagenesis of other agents, environmental or endogenous, that induce oxidative stress.