Genotoxic exposure to chemical substances is common, and nursing mothers could transmit harmful substances or their metabolites to their offspring through breast milk. We explored the possibility of determining genotoxic effects in the erythrocytes of breastfeeding rat pups whose mothers received a genotoxic compound while nursing. Ten groups of female rats and five pups per dam were studied. T...

The cellular response to DNA damage involves multiple pathways that work together to promote survival in the face of increased genotoxic lesions. Proteins in these pathways are often posttranslationally modified, either by small groups such as phosphate, or by protein modifiers such as ubiquitin or SUMO. The recent discovery of many more SUMO substrates that are modified at higher levels in dam...

DNA double-strand breaks (DSB) and blocked replication forks activate the DNA damage response (DDR), a signaling pathway marked by phosphorylation of histone 2AX (H2AX). The phosphorylated form, γH2AX, accumulates at the site of damage and can be detected as foci by immunocytochemistry. Therefore, γH2AX is a sensitive and robust biomarker of DNA damage, notably DSB. Cells from peripheral blood ...

Paving workers are exposed during road paving to several polycyclic aromatic hydrocarbons (PAHs) contained in asphalt fumes. In this study early genotoxic and oxidative effects of exposure to bitumen fumes were evaluated in 19 paving workers and 22 controls. Environmental and biological monitoring of exposure was carried out, measuring, on personal air samples from exposed workers collected dur...

Tobacco is a harmful genotoxic and mutagenic natural compound. It is genotoxic due to the chemical components contained in it like Nicotine ,phenols, benzene, carbon monoxide etc.,. Tobacco smokers are at risk of oral cancers due to the genotoxic nature of nicotine present in tobacco, which has the capacity to damage the DNA and alter its structure, finally resulting in the mutagenic and genoto...

While there is excellent concordance between the results of animal and human studies on known human carcinogens, the data are much less consistent for known animal carcinogens, There could be many reasons for this, First, there may have been inadequate study or length and magnitude of human exposure to demonstrate human susceptibility. A second major factor is the difference in the proportion o...

Polycyclic Aromatic Hydrocarbons (PAHs) constitute a family of over one hundred compounds and can generally be found in complex mixtures. PAHs metabolites cause DNA damage which can lead to the development of carcinogenesis. Toxicity assessment of PAH complex mixtures is currently expressed in terms of toxic equivalents, based on Toxicity Equivalent Factors (TEFs). However, the definition of ne...

In response to genotoxic insults, cells activate DNA damage response pathways that either stimulate transient cell cycle arrest and DNA repair or induce apoptosis. The Caenorhabditis elegans germ line is now well established as a model system to study these processes in a genetically tractable, multicellular organism. Upon treatment with genotoxic agents, premeiotic C. elegans germ cells transi...

The goals of genetic ecotoxicology are discussed and redefined. New directions in which genotoxicity "effect" studies might be pursued are outlined. Recognition of the genotoxic disease syndrome in lower animals suggests that more attention should be given to exploring the relationships between DNA damage (adduct formation, gene mutations, etc.) and its manifestation at the level of individuals...

DNA damage checkpoints delay mitotic cell-cycle progression in response to DNA stress, stalling the cell cycle to allow time for repair. CDKB is a plant-specific cyclin-dependent kinase (CDK) that is required for the G₂/M transition of the cell cycle. In Arabidopsis, DNA damage leads the degradation of CDKB2, and the subsequent G₂ arrest gives cells time to repair damaged DNA. G₂ arrest also tr...