Time-dependent post-exposure self-recovery rescues arsenic-induced behavioral and biochemical alterations in mice.
Source: PubMed, NCBI / U.S. National Library of Medicine
Chronic arsenic (As)-exposure leads to behavioral and biochemical changes both in humans and laboratory animals. However, post-exposure self-recovery after prolonged As-exposure remains unclear. This study evaluated the effects of As-exposure via drinking water (5 mg/kg body-weight/day) for 60 days and post-exposure self-recovery at 30-, 45-, and 60-days on behavioral and biochemical alterations in a mouse model. As-exposure mice exhibited augmented anxiety, impaired memory, and decreased motor coordination compared to controls. Furthermore, diminished cholinesterase and antioxidant environment, increased inflammation, and elevated Felevels were observed in brains of As-exposed mice. However, after stopping drinking As-contaminated water, recovery groups showed less anxiety, improved memory, and motor coordination. Moreover, levels of Nrf2 and GSH, and activities of SOD, HO-1, AChE, and BChE were significantly increased in brains of 45- and 60-day recovery groups compared to As-exposed group. Besides, remarkably reduced Feand MDA levels, concurrent with increased GPx4 activities in brains of the 45- and 60-day recovery groups, indicate attenuation of ferroptosis. Additionally, 45- and 60-day recovery groups showed decreased levels of IL-1β and IL-6, while increased IL-10 levels indicated reduced inflammation. These results suggest that stopping As-intake facilitates the attenuation of oxidative stress-mediated anxiety, cognitive, and motor coordination impairment in As-
Abstract
Chronic arsenic (As)-exposure leads to behavioral and biochemical changes both in humans and laboratory animals. However, post-exposure self-recovery after prolonged As-exposure remains unclear. This study evaluated the effects of As-exposure via drinking water (5 mg/kg body-weight/day) for 60 days and post-exposure self-recovery at 30-, 45-, and 60-days on behavioral and biochemical alterations in a mouse model. As-exposure mice exhibited augmented anxiety, impaired memory, and decreased motor coordination compared to controls. Furthermore, diminished cholinesterase and antioxidant environment, increased inflammation, and elevated Felevels were observed in brains of As-exposed mice. However, after stopping drinking As-contaminated water, recovery groups showed less anxiety, improved memory, and motor coordination. Moreover, levels of Nrf2 and GSH, and activities of SOD, HO-1, AChE, and BChE were significantly increased in brains of 45- and 60-day recovery groups compared to As-exposed group. Besides, remarkably reduced Feand MDA levels, concurrent with increased GPx4 activities in brains of the 45- and 60-day recovery groups, indicate attenuation of ferroptosis. Additionally, 45- and 60-day recovery groups showed decreased levels of IL-1β and IL-6, while increased IL-10 levels indicated reduced inflammation. These results suggest that stopping As-intake facilitates the attenuation of oxidative stress-mediated anxiety, cognitive, and motor coordination impairment in As-exposed mice.