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The genotoxic effect of potassium metabisulfite using chromosome aberration, sister chromatid exchange, micronucleus tests in human lymphocytes and chromosome aberration test in bone marrow cells of rats
Author(s) -
YavuzKocaman Ayse,
Rencuzogullari Eyyup,
Ila Hasan Basri,
Topaktas Mehmet
Publication year - 2008
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.20382
Subject(s) - sister chromatid exchange , micronucleus test , mitotic index , micronucleus , chromosome aberration , mutagen , bone marrow , microbiology and biotechnology , chemistry , cytotoxic t cell , genotoxicity , sister chromatids , chromatid , biology , immunology , carcinogen , chromosome , genetics , mitosis , toxicity , biochemistry , dna , in vitro , organic chemistry , gene
Potassium metabisulfite (PMB) is used as an antimicrobial substance in many kinds of foods. In the present study, the effects of PMB on chromosome aberrations (CAs), sister chromatid exchanges (SCEs), and micronucleus (MN) formation in human lymphocytes and as well as its effect on CAs in bone marrow cells of rats were investigated. The human lymphocytes were treated with 25, 50, 100, and 200 μg/ml of PMB for 24 and 48 hr. PMB was also intraperitoneally (ip) injected to the rats as a single dose of 150, 300, and 600 mg/kg body weight (b.w.) for 12 and 24 hr before sacrifice. PMB induced abnormalities such as structural and numerical (total) CAs, SCEs, and MN formations in a dose dependent manner in the lymphocytes of the 24‐ and 48‐hr treatment periods. In addition, PMB showed a cytotoxic effect by decreasing the replication index (RI), mitotic index (MI) and nuclear division index (NDI) in a dose dependent manner in human lymphocytes. The compound induced CA as well and decreased the MI in bone marrow cells of rats. It might be concluded that PMB had a high genotoxic and cytotoxic risk. Environ. Mol. Mutagen., 2008. © 2008 Wiley‐Liss, Inc.