Effect of Fluorosis on Liver Cells of VC Deficient and Wild Type Mice

Author:

Wei Wei12,Jiao Yan23,Ma Yonghui2,Stuart John M.45,Li Xiudian6,Zhao Fusheng23,Wang Lishi2,Sun DianJun1,Gu Weikuan2ORCID

Affiliation:

1. Center for Endemic Disease Control, Centers for Disease Control and Prevention, Institute of Endemic Fluorosis Disease, Harbin Medical University, Harbin, Heilongjiang 150081, China

2. Departments of Orthopaedic Surgery and BME, Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC), 956 Court Avenue, Memphis, TN 38163, USA

3. Mudanjiang Medical College, Mudanjiang, Heilongjiang 157001, China

4. Division of Connective Tissues Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA

5. Department of Veterans Affairs Medical Center, Memphis, TN 38104, USA

6. Department of Nephrology, Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, China

Abstract

For decades, mouse and other rodents have been used for the study of oxidative or related studies such as the effect of fluoride. It is known that rodents normally synthesize their own vitamin C (VC) due to the presence of a key enzyme in ascorbic acid synthesis, l-gulono-lactone-γ-oxidase (Gulo), while humans do not have the capacity of VC synthesis due to the deletion of most parts of the GULO gene. The spontaneous fracture (sfx) mouse recently emerged as a model for study of VC deficiency. We investigated the effect of fluoride on liver cells from wild type Balb/c andsfxmice. We found that activities of SOD, GPx, and CAT were reduced in both wild type andsfxmice; however, the amount of reduction in thesfxcells is more than that in Balb/c cells. In addition, while both cells increased MDA, the increase in thesfxcells is greater than that in Balb/c cells. Gene networks ofSod,Gpx, andCatin the liver of humans and mice are also different. Our study suggests that reaction to fluoride in vitamin C deficient mice might be different from that of wild type mice.

Funder

National Institute of Arthritis and Musculoskeletal and Skin Diseases

Publisher

Hindawi Limited

Subject

General Environmental Science,General Biochemistry, Genetics and Molecular Biology,General Medicine

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