| A systematic review of the carcinogenicity of rats and mice by sex due to exposure to phenyl compounds | 2024.12.31 | ||
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저자: Kyung？Taek Rim
Abstract
Objectives Diferences in cancer incidence between men and women are often explained by diferences in environmental exposure, or the infuence of sex hormones. However, there is little research on the intrinsic diferences in sensitivity to chemical carcinogens. Methods To predict and consider related in vivo carcinogenicity tests, changes in gene expression were examined in rats and mice (by gender and organ) due to exposure to carcinogenic chemicals such as phenyl compounds, which among chemicals are the main cause of carcinogenesis. Results In the case of male SD rats, the genes IL1B, TNF, NOS2, IL6, and NGF were related, and the probability of carcinogenesis in the urinary bladder, kidney, and oral cavity was high. In female SD rats, the genes ADRB2, TNF, HMOX1, CYP1A1, PTGS2, ILB1, CASP3, POR, PRL, TSC22D1, ATEG, REG1, HRH2, NFE2L2, AKR1C2, ADRB2, NR3C1, IL6, ADRB1, ADRB3, and LPO showed high probability of carcinogenesis in the stomach, liver, and nasal cavity. In the male F344 rat, the genes ACACA, ACSL1, ALB, ALCAM, CYP19A1, PPARA, CYP4A1, ACAA1, and ACOX1 were related, and showed a high probability of carcinogenesis in the liver, kidney, stomach, and urinary bladder. In the female F344 rat, no related genes were found, but a high probability of carcinogenesis was shown in the kidney, ear, Zymbal’s gland, stomach, and liver. In male ICR mice, no related genes and organs with a high probability of carcinogenesis were found, while in female ICR mice, genes for KRAS, ACHE, CAT, CYP3A4, and GPT were involved, and carcinogenesis occurred in the stomach, thyroid gland, ovary, liver, etc. The probability was shown to be high. In BALBc mice, no related genes and organs with a high probability of carcinogenesis were found, while in female BALBc mice, the genes NR1I2, CYP3A4, ABCB1, CYP2B6, PRKDC, CYP2C9, and NCOA1 were related, and the liver, etc., had a high probability of carcinogenesis. Conclusion Diferences in the epigenetics of each sex begin at the moment of fertilization due to diferences in sex chromosome gene expression and metabolic profles between XX and XY embryos. These fundamental sex diferences in nutrient utilization and mitochondrial activity may contribute to sex diferences in the metabolic reprogramming of cancer cells, which is important during cancer development, cancer progression, and response to anticancer treatment. Purpose of review In 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 fndings Diferences in the epigenetics of each sex begin at the moment of fertilization due to diferences in sex chromosome gene expression and metabolic profles between XX and XY embryos. Throughout development, additional processes, such as X-chromosome inactivation and gonadal steroid exposure, further distinguish the sexes.
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 다음글 |
Chemical toxicity by sex diferences: a literature review of 2019？2023 studies |