We for the first time explicitly show that arsenic exposure causes morphological damage to the thymus and results in heightened death of thymocytes.
Our data suggests that arsenic-induced apoptosis occurs due to increase in cellular oxidative and nitrosative stress.
We have for the first time established a non-classical role of NF-κB, correlating it with increase in FoxP3 expression.
The % of CD4+ CD25+ T cells were high and expression of FoxP3 has also increased at higher doses of arsenic indicating an nTreg bias.