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The Reversible Inhibition of Myoblast Proliferation by -Hexachlorocyclohexane¹

U.S. Department of Agriculture^,5, Clay Center, NE 68933

Abstract

The effects of treating non-fusing myoblast variants, fu-1 and M₃ A, with two levels (1 x 10^–4 M and 2 x 10^–4 M) of -hexachlorocyclohexane, an inhibitor of phosphatidylinositol synthesis, on myoblast proliferation were evaluated by measuring myoblast proliferation (counting cells) and visual inspection via phase microscopy. In the presence of -hexachlorocyclohexane, these cells were arrested, presumably in G₁. The inability of these cells to replicate did not appear to be due to a toxic effect of -hexachlorocyclohexane, because these cells were capable of resuming proliferation once they were transferred to media lacking -hexachlorocyclohexane. Cells were grown in media containing myo-[2-³ H] inositol and the radioactive content of water-soluble metabolites, the end product of phosphatidylinositides hydrolysis, was quantitated. Cells that were grown in the presence of -hexachlorocyclohexane, in addition to the loss of proliferative ability, also contained significantly less water-soluble metabolites. Therefore, it appears that there is a direct relationship between phosphatidylinositol metabolism and cell proliferation in the cell lines studied.

¹ Michigan Agr. Exp. Sta. Journal Article No. 11910.

² Postdoctoral Fellow, Dept. of Food Sci. and Human Nutr., Michigan State Univ., stationed at Roman L. Hruska U.S. Meat Anim. Res. Center, Clay Center, NE 68933.

³ Roman L. Hruska U.S. Meat Anim. Res. Center, Clay Center, NE 68933.

⁴ Dept. of Food Sci. and Human Nutr., Michigan State Univ., East Lansing, MI 48824.

⁵ Mention of a trade name, proprietary products or specific equipment does not constitute a guarantee or warranty of the product by the USDA and does not imply its approval to the exclusion of other products that may also be suitable.