Abstract
The contractile responses of isolated uterine segments from 17β-estradiol-3-benzoate-treated ovariectomized rats to acetylcholine (ACh) and high KCI in Ca-depleted modified Locke-Ringer solution on addition of CaCl2 were used as indicators of Ca2+ influxes through ACh receptor- and voltage-operated Ca2+ channels, respectively. L-Methionine (L-Met) significantly enhanced these responses. The enhancement depended on the time of treatment with L-Met and concentration of L-Met. 3-Deazaadenosine (3-DAA) plus homocysteine thiolactone (HCTL), which inhibit S-adenosylmethionine-dependent methylation, caused dose-dependent inhibition of these contractile responses to ACh and high KCI. These inhibitory effects of 3-DAA plus HCTL were significantly attenuated in the presence of L-Met. Protein carboxylmethyltransferase and phospholipid methyltransferase activities were detected in the isolated uterine segment under conditions similar to those in which the contractile responses were observed. 3-DAA plus HCTL inhibited these enzyme activities. These findings suggest that S-adenosylmethionine-dependent methylations of protein and/or phospholipid in isolated uterine segment are involved in the contractile responses to ACh and high KCI in Ca-depleted modified Locke-Ringer solution on addition of CaCl2.
