Deletion of IL-1β exacerbates acrylamide-induced neurotoxicity in mice

Author:

Fergany Alzahraa12,Zong Cai1,Ekuban Frederick Adams1ORCID,Suzuki Aina1,Kimura Yusuke1ORCID,Ichihara Sahoko3,Iwakura Yoichiro4,Ichihara Gaku1

Affiliation:

1. Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science , Noda, Japan

2. Laboratory of Genetics and Genetic Engineering in Department of Animal Husbandry and Animal Wealth Development, Faculty of Veterinary Medicine, Alexandria University , Alexandria, Egypt

3. Department of Environmental and Preventive Medicine, Jichi Medical University School of Medicine , Shimotsuke, Japan

4. Division of Experimental Animal Immunology, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Japan

Abstract

Abstract Acrylamide is a neurotoxicant in human and experimental animals. Interleukin-1β (IL-1β) is a proinflammatory cytokine known as a critical component of brain reaction to any insult or neurodegenerative pathologies, though its role in electrophile-induced neurotoxicity remains elusive. The aim of this study was to investigate the role of IL-1β in acrylamide-induced neurotoxicity in mice. Ten-week-old male wild-type and IL-1β knock-out mice were allocated into 3 groups each and exposed to acrylamide at 0, 12.5, 25 mg/kg body weight by oral gavage for 28 days. Compared with wild-type mice, the results showed a significant increase in landing foot spread test and a significant decrease in density of cortical noradrenergic axons in IL-1β KO mice exposed to acrylamide at 25 mg/kg body weight. Exposure to acrylamide at 25 mg/kg significantly increased cortical gene expression of Gclc, Gpx1, and Gpx4 in wild-type mice but decreased them in IL-1β KO mice. The same exposure level significantly increased total glutathione and oxidized glutathione (GSSG) in the cerebellum of wild-type mice but did not change total glutathione and decreased GSSG in the cerebellum of IL-1β KO mice. The basal level of malondialdehyde in the cerebellum was higher in IL-1β KO mice than in wild-type mice. The results suggest that IL-1β protects the mouse brain against acrylamide-induced neurotoxicity, probably through suppression of oxidative stress by glutathione synthesis and peroxidation. This unexpected result provides new insight on the protective role of IL-1β in acrylamide-induced neurotoxicity.

Funder

Japan Society for the Promotion of Science

Publisher

Oxford University Press (OUP)

Subject

Toxicology

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