Adebiyi Adebowale, Adaikan P Ganesan, Prasad R N V
Department of Obstetrics and Gynaecology, National University of Singapore, National University Hospital, 119074, Singapore.
Pharmacol Res. 2004 May;49(5):415-22. doi: 10.1016/j.phrs.2003.10.011.
The present study examines the effect of benzyl isothiocyanate (BITC) on uterine contraction in vitro. BITC (10-320 microM) caused irreversible, concentration-dependent inhibition of the spontaneous, prostaglandin F(2alpha) (PGF(2alpha)) and oxytocin-induced force of gravid and non-gravid rat uterine contractions in contrast to equivalent concentrations of DMSO (solvent control). At 160 microM of BITC, spontaneous, PGF(2alpha) and oxytocin-induced force of gravid rat myometrial contractions were reduced to 16 +/- 6%, 15 +/- 7 % and 17 +/- 4% (of the control contractions), respectively. Moreover, at 320 microM of BITC, spontaneous, PGF(2alpha) and oxytocin-induced force of non-gravid rat uterine contractions were reduced to 10+/-5 %, 4+/-1 % and 7+/-2 % (of the control contractions), respectively. Incubation of isolated non-gravid rat uterine strips in Ringer Locke solution containing 100 microM of BITC for 1h prior to recording their activity also caused significant and irreversible depression of KCl (60mM)-induced tension development in the uterus relative to the solvent control (P < 0.01). In 56% of BITC-pretreated uterine tissues, spontaneous contractions were totally abolished. Cryosections of BITC-treated uterus (hematoxyline and eosin stained) examined under light microscope revealed structural disintegrity with marked vacuolar degeneration of the endometrium and myometrium. It thus appears that like the vascular smooth muscle (reported by previous workers), BITC is also capable of causing functional aberration of isolated uterus by provoking degeneration of the myometrium.
本研究考察了异硫氰酸苄酯（BITC）对体外子宫收缩的影响。与同等浓度的二甲基亚砜（溶剂对照）相比，BITC（10 - 320微摩尔）对妊娠和未妊娠大鼠子宫的自发收缩、前列腺素F2α（PGF2α）和催产素诱导的收缩力产生不可逆的、浓度依赖性抑制。在160微摩尔的BITC作用下，妊娠大鼠子宫肌层的自发收缩、PGF2α和催产素诱导的收缩力分别降至对照收缩力的16±6%、15±7%和17±4%。此外，在320微摩尔的BITC作用下，未妊娠大鼠子宫的自发收缩、PGF2α和催产素诱导的收缩力分别降至对照收缩力的10±5%、4±1%和7±2%。在记录分离的未妊娠大鼠子宫条活性前，将其在含有100微摩尔BITC的林格洛克溶液中孵育1小时，相对于溶剂对照，也导致子宫对氯化钾（60毫摩尔）诱导的张力发展产生显著且不可逆的抑制（P < 0.01）。在56%的经BITC预处理的子宫组织中，自发收缩完全消失。在光学显微镜下检查经BITC处理的子宫（苏木精和伊红染色）冰冻切片，发现结构完整性受损，子宫内膜和子宫肌层有明显的空泡变性。因此，与先前研究人员报道的血管平滑肌情况类似，BITC似乎也能够通过引发子宫肌层变性而导致离体子宫功能异常。
