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Archives of Clinical Toxicology
ISSN: 2692-8280
Kartoosh Heydari
Director
UC Berkeley, USA
Non-alcoholic fatty liver disease: Role of PNPLA3 and its association with environmental chemicals
Toxicological assessment of chondroitin sulfate oligosaccharide
RAD51 Inhibitor Reverses Etoposide-Induced Genomic Toxicity and Instability in Esophageal Adenocarcinoma Cells
Archives of Clinical Toxicology is an international peer reviewed open access journal that publishes most elevated quality unique logical research and basic surveys on systems of lethality related with exposures to outside synthetic compounds. The aim of the journal is to advance current understanding about toxicity particularly related to human health. The journal addresses both scientific research and clinical advances in clinical toxicology.
Molds and mycotoxins indoors I: Current issues and way forward
Molds grow from microscopic spores of many fungi floating in the air and when land on surfaces that are moist; none of the molds grow in the absence of moisture [1,2]. Molds are ubiquitous and found both outdoors and indoors. Outdoors, molds play a vital role in the breakdown of dead organic matters like fallen leaves and dead trees.
Molds and mycotoxins indoors III: Three case reports
Molds are microscopic fungi which are one of the most diverse and abundant eukaryotes. Not all fungi produce molds, some produce mushrooms and others grow as single cells like yeasts. Molds are ubiquitous, both outdoors and indoors. Certain molds produce mycotoxins that can cause many adverse health effects, especially in immunocompromised and/or genetically predisposed individuals.
Environmental risk assessment (ERA)
ERA is a robust tool in environmental decision-making, offering a quantitative framework for risk assessment and management. By separating scientific analysis from policymaking, ERA ensures objective evaluations of ecological risks. Whether dealing with prospective risks or retrospective assessments of past environmental damage, ERA provides a means to balance ecological protection with economic and social considerations.
Perinatal polychlorinated biphenyls disrupt`the TRH-TSH axis in the adult female rat: A morphometric immunocytochemical study
Polychlorinated Biphenyls (PCBs) are endocrine disruptors that may act as thyroid hormone (TH) analogues/antagonists to alter the homeostasis of the thyroid axis. Recently, we have shown that perinatal exposure to Aroclor 1254 (A1254), a commercial mixture of more than 90 PCB congeners, leads to sex-specific changes of the thyrotropin-releasing hormone (TRH) mRNA synthesis in hypophysiotropic neurons of the hypothalamic paraventricular nucleus (PVN), and thyroid-stimulating hormone (TSH) serum levels in adult rats.
Toxicological assessment of anandamide
Anandamide (AEA), an endogenous cannabinoid, has been widely studied for its physiological roles and potential therapeutic applications. However, concerns remain regarding its safety profile, particularly at higher doses. Therefore, this study aimed to investigate the acute, subchronic and genetic toxicological effects of AEA.
Molds and mycotoxins indoors II: Toxicological perspective
Fungal infections are among the most difficult diseases to diagnose and manage and can cause significant morbidity and mortality. It is estimated that globally, fungal infections occur in at least 13 million people and cause more than 1.5 million deaths every year, costing billions of dollars. Out of millions of fungal species, only several hundred species cause diseases among humans, primarily in immunocompromised and critically ill individuals, and only a very few fungal species can affect healthy individuals.
An analysis of racial disparities in systemic treatments for psoriasis and their pharmacologic consequences
Psoriasis is a systemic inflammatory skin disease associated with significant comorbidities, yet access to effective systemic treatments remains disparate across racial and ethnic groups. Building upon recent findings of disparities in systemic medication prescriptions and hospitalization outcomes among patients with psoriasis, this commentary explores the pharmacologic, toxicologic, and health equity implications of these inequities.
Non-alcoholic fatty liver disease: Role of nuclear receptor superfamily members and approaches to treatment
Non-alcoholic fatty liver disease (NAFLD) is an increasing health problem when left untreated. NAFLD is defined as accumulation of fat in 5% of the hepatocytes. NAFLD can convert into non-alcoholic steatohepatitis (NASH) which is defined as inflammatory NAFLD. Both NAFLD and NASH are observed in individuals suffering from metabolic syndrome and type 2 diabetes (T2D).
Non-alcoholic fatty liver disease: Role of PNPLA3 and its association with environmental chemicals
Non-alcoholic fatty liver disease (NAFLD) represents an escalating global health concern. Its prevalence varies significantly across different regions, in Asia it ranges from 30-32%, with notably higher prevalence in the Middle East. Europe reports a prevalence of 27-33%, while North America shows a range of 35-48%.
RAD51 Inhibitor Reverses Etoposide-Induced Genomic Toxicity and Instability in Esophageal Adenocarcinoma Cells
In normal cells, homologous recombination (HR) is strictly regulated and precise and plays an important role in preserving genomic integrity by accurately repairing DNA damage. RAD51 is the recombinase which mediates homologous base pairing and strand exchange during DNA repair by HR. We have previously reported that HR is spontaneously elevated (or dysregulated) in esophageal adenocarcinoma (EAC) and contributes to ongoing genomic changes and instability. The purpose of this study was to evaluate the impact of RAD51 inhibitor on genomic toxicity caused by etoposide, a chemotherapeutic agent.
Non-alcoholic fatty liver disease: Role of nuclear receptor superfamily members and approaches to treatment
Non-alcoholic fatty liver disease (NAFLD) is an increasing health problem when left untreated. NAFLD is defined as accumulation of fat in 5% of the hepatocytes. NAFLD can convert into non-alcoholic steatohepatitis (NASH) which is defined as inflammatory NAFLD. Both NAFLD and NASH are observed in individuals suffering from metabolic syndrome and type 2 diabetes (T2D).
Valproate, Topiramate, and emerging neurodevelopmental concerns
Our brain is the most intricated organ of our body. It is, therefore, unsurprising that external factors to which the fetus is exposed to during its development, such as drugs, alcohol, environmental toxicants, and medicines may have lasting effects that extend into adulthood [1,2].
Non-alcoholic fatty liver disease: Role of nuclear receptor superfamily members and approaches to treatment
Non-alcoholic fatty liver disease (NAFLD) is an increasing health problem when left untreated. NAFLD is defined as accumulation of fat in 5% of the hepatocytes. NAFLD can convert into non-alcoholic steatohepatitis (NASH) which is defined as inflammatory NAFLD. Both NAFLD and NASH are observed in individuals suffering from metabolic syndrome and type 2 diabetes (T2D).
Valproate, Topiramate, and emerging neurodevelopmental concerns
Our brain is the most intricated organ of our body. It is, therefore, unsurprising that external factors to which the fetus is exposed to during its development, such as drugs, alcohol, environmental toxicants, and medicines may have lasting effects that extend into adulthood [1,2].
RAD51 Inhibitor Reverses Etoposide-Induced Genomic Toxicity and Instability in Esophageal Adenocarcinoma Cells
In normal cells, homologous recombination (HR) is strictly regulated and precise and plays an important role in preserving genomic integrity by accurately repairing DNA damage. RAD51 is the recombinase which mediates homologous base pairing and strand exchange during DNA repair by HR. We have previously reported that HR is spontaneously elevated (or dysregulated) in esophageal adenocarcinoma (EAC) and contributes to ongoing genomic changes and instability. The purpose of this study was to evaluate the impact of RAD51 inhibitor on genomic toxicity caused by etoposide, a chemotherapeutic agent.