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Title: Effect of benzyl isothiocyanate on spontaneous and induced force of rat uterine contraction
Authors: Adebiyi, A.
Adaikan, P.G. 
Prasad, R.N.V. 
Keywords: Benzyl isothiocyanate
Smooth muscle
Uterine contraction
Issue Date: 2004
Citation: Adebiyi, A., Adaikan, P.G., Prasad, R.N.V. (2004). Effect of benzyl isothiocyanate on spontaneous and induced force of rat uterine contraction. Pharmacological Research 49 (5) : 415-422. ScholarBank@NUS Repository.
Abstract: The present study examines the effect of benzyl isothiocyanate (BITC) on uterine contraction in vitro. BITC (10-320μM) caused irreversible, concentration-dependent inhibition of the spontaneous, prostaglandin F 2α (PGF2α) and oxytocin-induced force of gravid and non-gravid rat uterine contractions in contrast to equivalent concentrations of DMSO (solvent control). At 160μM of BITC, spontaneous, PGF2α 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 320μM of BITC, spontaneous, PGF2α 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 100μM 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. © 2003 Elsevier Ltd. All rights reserved.
Source Title: Pharmacological Research
ISSN: 10436618
DOI: 10.1016/j.phrs.2003.10.011
Appears in Collections:Staff Publications

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