Journal of Biochemical and Molecular Toxicology

Volume 31, Issue 7 e21906

RESEARCH ARTICLE

Protective effect of hydroxytyrosol in arsenic-induced mitochondrial dysfunction in rat brain

Manisha Soni,

Manisha Soni

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

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Chandra Prakash,

Chandra Prakash

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

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Sfurti Sehwag,

Sfurti Sehwag

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

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Vijay Kumar,

Corresponding Author

Vijay Kumar

[email protected]

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

Correspondence Vijay Kumar. Email: [email protected]Search for more papers by this author

Manisha Soni,

Manisha Soni

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

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Chandra Prakash,

Chandra Prakash

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

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Sfurti Sehwag,

Sfurti Sehwag

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

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Vijay Kumar,

Corresponding Author

Vijay Kumar

[email protected]

Department of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001 India

Correspondence Vijay Kumar. Email: [email protected]Search for more papers by this author

First published: 22 February 2017

https://doi.org/10.1002/jbt.21906

Citations: 24

Contract Grant Sponsor: Indian Council of Medical Research, New Delhi, India.

Contract Grant Number: 58/51/2011-BMS.

Contract Grant Sponsor: Department of Science and Technology, New Delhi, India.

Contract Grant Number: SR/FST/LSI-534/2012.

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Abstract

The present study was planned to investigate the protective effect of hydroxytyrosol (HT) against arsenic (As)-induced mitochondrial dysfunction in rat brain. Rats exposed to sodium arsenite (25 ppm for 8 weeks) showed decreased mitochondrial complexes (I, II, IV) activities, mitochondrial superoxide dismutase (MnSOD), and catalase activities in brain mitochondria. As-treated rats showed reduced mRNA expression of complex I (ND-1, ND-2), IV (COX-1, COX-4) subunits, and uncoupling protein-2 (UCP-2). In addition to this, As exposure downregulated the protein expression of MnSOD. Administration of HT with As restored the enzymatic activities of mitochondrial complexes, MnSOD and catalase, increased the mRNA levels of complexes subunits and UCP-2 as well as proteins level of MnSOD. These results suggest that HT efficiently restores mitochondrial dysfunction in As neurotoxicity and might be used as potential mitoprotective agent in future.

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Volume31, Issue7

July 2017

e21906

Protective effect of hydroxytyrosol in arsenic-induced mitochondrial dysfunction in rat brain

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Protective effect of hydroxytyrosol in arsenic-induced mitochondrial dysfunction in rat brain

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