Diphenylmethyl selenocyanate attenuates malachite green induced oxidative injury through antioxidation & inhibition of DNA damage in mice
Jayanta Kumar Das1, Sibani Sarkar2, Sk Ugir Hossain3, Pramita Chakraborty4, Rajat Kumar Das4, Sudin Bhattacharya4
1 Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, Kolkata, India and Present address:. Department of Environment and Occupational Health, Florida International University, 11200S.W. 8th St, University Park, AHC1, Room#413, Miami, FL 33199, USA
2 Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, Kolkata, India and Present address: Drug Development Diagnostics & Biotechnology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India
3 Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, Kolkata, India and Present address: Natural Plant Product Division, CSIR-Institute of Himalayan Bioresource Technology, Palampur, India
4 Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, Kolkata, India
Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India
Source of Support: None, Conflict of Interest: None
Background & objectives: Malachite green (MG), an environmentally hazardous material, is used as a non permitted food colouring agent, especially in India. Selenium (Se) is an essential nutritional trace element required for animals and humans to guard against oxidative stress induced by xenobiotic compounds of diverse nature. In the present study, the role of the selenium compound diphenylmethyl selenocyanate (DMSE) was assessed on the oxidative stress (OS) induced by a food colouring agent, malachite green (MG) in vivo in mice.
Methods: Swiss albino mice (Mus musculus) were intraperitoneally injected with MG at a standardized dose of 100 μg/ mouse for 30 days. DMSE was given orally at an optimum dose of 3 mg/kg b.w. in pre (15 days) and concomitant treatment schedule throughout the experimental period. The parameters viz. ALT, AST, LPO, GSH, GST, SOD, CAT, GPx, TrxR, CA, MN, MI and DNA damage have been evaluated.
Results: The DMSE showed its potential to protect against MG induced hepatotoxicity by controlling the serum alanine aminotransferase and aspartate amino transferase (ALT and AST) levels and also ameliorated oxidative stress by modulating hepatic lipid peroxidation and different detoxifying and antioxidative enzymes such as glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and also the selenoenzymes such as glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) and reduced glutathione level which in turn reduced DNA damage.
Interpretation & conclusions: The organo-selenium compound DMSE showed significant protection against MG induced heptotoxicity and DNA damage in murine model. Better protection was observed in pretreatment group than in the concomitant group. Further studies need to be done to understand the mechanism of action.