Affiliation:
1. Laboratorio de Antimutagénesis, Anticarcinogénesis y Antiteratogénesis Ambiental, Facultad de Estudios Superiores—Zaragoza Universidad Nacional Autónoma de México (UNAM) Mexico City Mexico
2. Department of Pharmacology, Faculty of Medicine, Neuroscience Center & Helsinki Institute of Life Science University of Helsinki Helsinki Finland
3. McLaughlin Centre for Population Health Risk Assessment University of Ottawa Ottawa Ontario Canada
Abstract
AbstractThis study investigated the genotoxic effects of chromium (Cr) in Hsd:ICR mice, considering factors such as oxidative state, apoptosis, exposure pathway, duration, pregnancy, and transplacental exposure. Genotoxicity was assessed using the erythrocytes' micronucleus (MN) assay, while apoptosis was evaluated in nucleated blood cells. The results showed that Cr(III) (CrK(SO4)2 and CrCl3) did not induce any marked genotoxic damage. However, Cr(VI) (CrO3, K2Cr2O7, Na2Cr2O7, and K2CrO4) produced varying degrees of genotoxicity, with CrO3 being the most potent. MN frequencies increased following 24‐h exposure, with a greater effect in male mice. Administering 20 mg/kg of CrO3 via gavage did not lead to significant effects compared to intraperitoneal administration. Short‐term oral treatment with a daily dose of 8.5 mg/kg for 49 days elevated MN levels only on day 14 after treatment. Pregnant female mice exposed to CrO3 on day 15 of pregnancy exhibited reduced genotoxic effects compared to nonpregnant animals. However, significant increases in MN levels were found in their fetuses starting 48 h after exposure. In summary, data indicate the potential genotoxic effects of Cr, with Cr(VI) forms inducing higher genotoxicity than Cr(III). These findings indicate that gender, exposure route, and pregnancy status might influence genotoxic responses to Cr.
Funder
Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México