A systematic review of the carcinogenicity of rats and mice by sex due to exposure to phenyl compounds

ConclusionDifferences in the epigenetics of each sex begin at the moment of fertilization due to differences in sex chromosome gene expression and metabolic profiles between XX and XY embryos. These fundamental sex differences in nutrient utilization and mitochondrial activity may contribute to sex differences in the metabolic reprogramming of cancer cells, which is important during cancer development, cancer progression, and response to anticancer treatment.Purpose of reviewIn this study, I compared and considered the degree of toxicity and genome expression in each male and female gender and organ due to exposure to phenyl compounds (PAH, etc.), which are the basis of benzene toxicity as aromatic hydrocarbons, and conducted future inhalation toxicity tests and related carcinogenicity tests.Recent findingsDifferences in the epigenetics of each sex begin at the moment of fertilization due to differences in sex chromosome gene expression and metabolic profiles between XX and XY embryos. Throughout development, additional processes, such as X-chromosome inactivation and gonadal steroid exposure, further distinguish the sexes.
Source: Molecular and Cellular Toxicology - Category: Cytology Source Type: research