Ansuman Chattopadhyay
Radiation Genetics and Chemical Mutagenesis Laboratory, India
Posters-Accepted Abstracts: J Cytol Histol
Fluoride (F) toxicity is a major threat to millions of people all over the world including India. It causes skeletal fluorosis as well as affects soft tissues. Fluoride is also reported to be genotoxic in human and other mammals though contradictory findings exist. We reported that even at equivalent dose of naturally prevailing concentrations, sodium fluoride (NaF) exerts significant genotoxicity to mouse bone marrow cells (BMCs). Interestingly the genotoxicity was not dose dependent showing the highest effect at 7.5-15 mg NaF/L which is equivalent to 3.4-6.8 mg F ion/L. We also reported that a significant level of reactive oxygen species (ROS) is generated in NaF treated mouse BMCs. Decreased level of glutathione, glutathione-Stransferase and increased lipid peroxidation supported that F-induced toxicityis mainly mediated via ROS generation. NaFtreatment also exhibited a higher population of Annexin-V positive cells. Till date the molecular mechanism of F-toxicity is not fully understood. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a transcription factor which binds to the anti oxidant responsive elements of antioxidant genes and therefore may play a major regulatory role in F-induced genotoxicity. We therefore attempted to study the expression pattern of some of these antioxidant genes viz. glutathione reductase, heme oxygenase1, NADPH Quinone Oxidase1 related to Nrf2 signaling pathway as well as Hsp70, glutathione-S-transferase and gamma glutamyltransferase. The expression pattern of Kelch-like ECH-associated protein 1, an inhibitor of Nrf2 was also monitored simultaneously. The expression pattern of these genes will be discussed to understand the role of Nrf2 in F-induced genotoxicity.
Email: chansuman1@rediffmail.com
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