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Modulation of Acid Phosphatase and Lactic Dehydrogenase in Hexachlorocyclohexane‐Induced Hepatocarcinogenesis in Mice
Author(s) -
Bhatt Devendra Kumar,
Nagda Girima
Publication year - 2012
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21441
Subject(s) - acid phosphatase , lactate dehydrogenase , alkaline phosphatase , metastasis , enzyme , oxidative stress , chemistry , hexachlorocyclohexane , lactic acid , phosphatase , medicine , endocrinology , biochemistry , pathology , biology , cancer , bacteria , genetics , pesticide , agronomy
ABSTRACT The present study was designed to elucidate the involvement of acid phosphatase (ACP) in metastasis and lactate dehydrogenase (LDH) as an immediate compensatory alleviation mechanism for energy stress in liver lesions induced by hexachlorocyclohexane in Swiss mice. Animals were continuously exposed to hexachlorocyclohexane (500 ppm) for 2, 4, and 6 months. Neoplastic nodules and tumors developed after continuous exposure for 4 and 6 months, respectively. The distribution pattern of both enzymes markedly varied in neoplastic nodules and tumors. Intense ACP activity was more observed only in sinusoids and blood vessels of neoplastic nodule, whereas an overall increase in ACP activity was observed in the tumor. Noticeably, a significant decline in LDH activity was noted after 2 and 4 months of exposure, whereas LDH in a tumor region showed intense enzymatic activity. The role of acid phosphate in metastasis and LDH in oxidative stress during hepatocarcinogenesis induced by hexachlorocyclohexane has been discussed. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:439‐444, 2012; View this article online at wileyonlinelibrary.com . DOI 10:1002/jbt.21441