RESUMEN
Mercury is widely used in industrial and extractive processes, and the improper disposal of waste or products containing this metal produces a significant impact on ecosystems, causing adverse effects on living organisms, including humans. Exposure to methylmercury, a highly toxic organic compound, causes important neurological and developmental impairments. Recently, the genotoxicity of mercurial compounds has gained prominence as one of the possible mechanisms associated with the neurological effects of mercury, mostly by disturbing the mitotic spindle and causing chromosome loss. In this sense, it is important to investigate if these compounds can also cause direct damage to DNA, such as single and double-strand breaks. Thus, the aim of this study was to investigate the cytotoxic and genotoxic potential of methylmercury in cell lines derived from neurons (B103) and glia (C6), exposed to methylmercury (MeHg) for 24 h, by analyzing cell viability, metabolic activity, and damage to DNA and chromosomes. We found that in comparison to the neuronal cell line, glial cells showed higher tolerance to MeHg, and therefore a higher LC50 and consequent higher intracellular accumulation of Hg, which led to the occurrence of several genotoxic effects, as evidenced by the presence of micronuclei, bridges, sprouts, and chromosomal aberrations.
Asunto(s)
Mercurio , Compuestos de Metilmercurio , Daño del ADN , Ecosistema , Humanos , Compuestos de Metilmercurio/metabolismo , Compuestos de Metilmercurio/toxicidad , Neuroglía/metabolismoRESUMEN
ABSTRACT: The ongoing coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 has significant implications in patients with concomitant cardiovascular disease (CVD) because they are the population at the greatest risk of death. The treatment of such patients and complications may represent a new challenge for the fields of cardiology and pharmacology. Thus, understanding the involvement of this viral infection in CVD might help to reduce the aggressiveness of SARS-CoV-2 in causing multiorgan infection and damage. SARS-CoV-2 disturbs the host epigenome and several epigenetic processes involved in the pathophysiology of COVID-19 that can directly affect the function and structure of the cardiovascular system (CVS). Hence, it would be relevant to identify epigenetic alterations that directly impact CVS physiology after SARS-CoV-2 infection. This could contribute to the view of this virus-induced CVS injury and direct forthcoming tackles for COVID-19 treatment to reduce mortality in patients with CVD. Targeting epigenetic marks could offer strong evidence for the development of novel antiviral therapies, especially in the context of COVID-19-related CVS damage. In this review, we address some of the main signaling pathways that are currently known as being involved in COVID-19 pathophysiology and the importance of this glint on epigenetics and some of its modifiers (epidrugs) to control the unregulated epitope activity in the context of SARS-CoV-2 infection, COVID-19, and underlying CVD.