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Sodium chlorate, a major water disinfection byproduct, alters brush border membrane enzymes, carbohydrate metabolism and impairs antioxidant system of Wistar rat intestine
Author(s) -
Ali Shaikh Nisar,
Ansari Fariheen Aisha,
Khan Aijaz Ahmed,
Mahmood Riaz
Publication year - 2017
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22388
Subject(s) - antioxidant , chemistry , malondialdehyde , brush border , oxidative stress , glutathione , small intestine , enzyme , biochemistry , chlorate , carbohydrate metabolism , metabolism , sodium hypochlorite , membrane , inorganic chemistry , vesicle , organic chemistry
Abstract Sodium chlorate (NaClO 3 ) is a widely used nonselective herbicide. It is also generated as a by‐product during disinfection of drinking water by chlorine dioxide. The purpose of this study was to evaluate the effect of NaClO 3 on rat intestine. Adult male rats were randomly divided into five groups: control and remaining four groups were administered orally different doses of NaClO 3 and sacrificed 24 h after the treatment. The administration of NaClO 3 produced acute oxidative stress in the intestine, which manifested in the form of markedly enhanced malondialdehyde levels and carbonyl content and lowered total sulfhydryl groups and glutathione levels. The activities of several brush border membrane (BBM) enzymes were greatly reduced as compared to control. There were alterations in the activities of various enzymes of carbohydrate metabolism and those involved in maintaining the antioxidant defense system. Histological studies support the biochemical results showing NaClO 3 dose‐dependent increase in tissue damage. Thus, the present study shows that oral administration of NaClO 3 decreases the activities of BBM enzymes, induces oxidative stress, alters metabolic pathways, and impairs the antioxidant system of rat intestine. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1607–1616, 2017.