Effect of lead on proliferation, oxidative stress and genotoxic damage of 3T3-L1 fibroblasts.

Lead (Pb) is an environmental and industrial contaminant that still represents a public health problem. In this paper, we investigated the effect of Pb on proliferation, lipid peroxidation and the number of micronucleated cells in exponentially growing 3T3-L1 fibroblasts, a cell line previously used to evaluate different environmental contaminants. We found that Pb (10 μM or higher) was able to inhibit proliferation of exponentially growing cells after 24-h treatment, which was evaluated by the MTT assay and cell counting in Neubauer chamber, but cell survival was not affected according to the trypan blue exclusion assay.

Lead enhancement of 3T3-L1 fibroblasts differentiation to adipocytes involves ERK, C/EBPβ and PPARγ activation.

Lead (Pb) is an environmental and industrial contaminant that still represents a public health problem. Elevated Pb exposure has been inversely correlated with femoral bone density and associated with osteoporosis. In the last years, it has been shown that inhibition of osteogenesis from mesenchymal stem cells activates adipogenesis and vice versa.

ACTH stimulates the release of alkaline phosphatase through Gi-mediated activation of a phospholipase C and the release of inositol-phosphoglycan.

We have previously reported that ACTH activates a phospholipase C that hydrolyzes glycosylphosphatidylinositol (GPI), which would release inositolphosphoglycan (IPG) to the extracellular medium, and that an IPG purified from Trypanosoma cruzi is able to inhibit ACTH-mediated steroid production in adrenocortical cells. In the present paper, it was found that anti-inositolphosphoglycan antibodies (anti-CRD) increased ACTH-mediated corticosterone production, which indicates that an endogenous IPG is a physiological inhibitor of ACTH response. On the other hand, we investigated the release to the extracellular medium of the GPI-anchored enzyme, alkaline phosphatase, by ACTH.