Polychlorinated biphenyls (PCBs) are molecules structurally related to dioxins and were widely used in the past in industrial applications. Their chemical stability and high lipophilicity make them persistent pollutants and dangerous occupational contaminants. Our previous results showed that "low concentrations" of PCBs (≤ 10 µg/ml, using the commercial mixture Aroclor 1254) inhibit in vitro hormonal induced myogenic differentiation. Here we extend the notion of PCBs as inhibitors of myogenic differentiation induced by lower serum medium. Aroclor 1254 treatment of myogenic cells, induced to differentiate in low serum medium, inhibits (at concentrations ≤ 10 µg/ml) the extent of fusion and the size of the myotubes as well as the accumulation of sarcomeric myosin. We also investigated whether the cell mortality observed at Aroclor 1254 concentrations ≥ 10 µg/ml is due to necrosis or to apoptosis. Using different approaches, we observed that Aroclor 1254 causes necrosis but not apoptosis of myogenic cells in a dose-dependent manner. In addition, we report that Aroclor 1254 induces release of the intracellular enzymes lactate dehydrogenase (LDH) and creatine kinase (CK) in a dose-dependent manner. These results may explain the CK serum elevation observed in patients exposed to high doses of PCBs.
Ionic channel proteins are possible sites of microwave interaction at the cell membrane level. Patch-clamp data, using single channel and total current recording, indicated that low level microwave fields may modify some functional parameters of the nicotinic acetylcholine receptor in primary chick myotubes, suggesting a possible effect of microwaves on myogenic cells. Here, we investigated the biological relevance of such results, in relation to the possible involvement of intracellular signaling processes. We exposed L6-C5 myogenic cells to low power electromagnetic fields and observed the consequences on hormonal activation of phospholipases C and D. We found that increased inositol phospholipid turnover, induced by acetylcholine and arginine vasopressin activation of phospholipase C, was not modified in microwave irradiated myoblasts or myotubes. Moreover, vasopressin-dependent phospholipase D activation, assessed by measuring the [3H]-free choline release, was not modified by microwave irradiation. Our conclusions suggest that low level microwave fields do not modify signal transduction pathways activated by acetylcholine and vasopressin in L6-C5 myogenic cells.
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