High impact information on ethylsulfanylmethanimidamide

• Brief intrapulmonary infusions of AG (140 mg), AMT (0.12 mg), and EIT (0.12 mg) increased basal PVR by 82, 69, and 77%, respectively (P < 0.05) [1].
• Crystal structures of human endothelial nitric oxide synthase (eNOS) and human inducible NOS (iNOS) catalytic domains were solved in complex with the arginine substrate and an inhibitor S-ethylisothiourea (SEITU), respectively [2].
• S-Ethylisothiourea was not a detectable substrate for eNOS [3].
• Three of the Type I ligands, S-ethylisothiourea, L-canavanine and 2,5-lutidine, displaced the CO from the haem iron upon addition to the iNOS oxygenase domain [4].
• In contrast, the amplitude of the constrictions of mesenteric arterioles induced by S-ethylisothiourea, an inducible NOS (iNOS) inhibitor, was significantly greater in the diabetic rats than in the control [5].

Biological context of ethylsulfanylmethanimidamide

• OBJECTIVES: To investigate the effects of S-ethylisothiourea (S-EITU) on hemodynamics, oxygen transport, and regional blood flow in healthy and septic sheep [6].
• S-ethylisothiourea, a nonamino acid inhibitor of nitric oxide synthase, reverses septic vasodilation in sheep [7].
• IP administration of isothioureas increased mean arterial blood pressure of the urethane-anaesthetised mouse (rank order of effect: IPTU > ETU > SMT > AETU) [8].
• Effect of S-ethylisothiourea, a putative inhibitor of inducible nitric oxide synthase, on mouse skin vascular permeability [9].
• Ethylisothiourea, an inhibitor of nitric oxide synthase, inhibited apoptosis induction by gp120 [10].

Anatomical context of ethylsulfanylmethanimidamide

• EITU was found to inhibit NO production by activated macrophages without interfering with the induction of iNOS [11].
• S-Ethylisothiourea (500-1000 microM), an inhibitor of nitric oxide synthase (NOS), significantly increased myotube injury and reduced nitric oxide (NO) in cultures consisting of only myotubes [12].
• Effect of a nitric oxide synthase inhibitor, S-ethylisothiourea, on cultured cells and cardiovascular functions of normal and lipopolysaccharide-treated rabbits [13].

Associations of ethylsulfanylmethanimidamide with other chemical compounds

• The approximate EC50 values as inhibitors of NO production, assessed by 24-h accumulation in cell culture media, were 10 microM (EITU), 30 microM (AEITU), 300 microM (NG-methylarginine), and 1000 microM (aminoguanidine) [11].
• Only the N-acetylurea and urea corresponding to NCD-4 are appreciably fluorescent: the O-phenylisourea and S-ethylisothiourea derivatives have negligible fluorescence [14].
• Exposure of the cultured cells to S-ethylisothiourea (1 mmol l(-1)), a selective inhibitor of iNOS, suppressed the production of NO by 63%, PGE by 69% and progesterone by 48% [15].

Gene context of ethylsulfanylmethanimidamide

• The NOS inhibitor ethylisothiourea, used for control purposes, showed a hypertensive effect in eNOS+/+ mice, but no such effect in eNOS-/- mice [16].

Analytical, diagnostic and therapeutic context of ethylsulfanylmethanimidamide

• 1. The aim of this study was to compare the effects of an intravenous infusion of a potent and non selective nitric oxide synthase inhibitor S-ethylisothiourea (Ethyl-TU) with that of a nitric oxide (NO) donor on the pathological sequelae associated with splanchnic artery occlusion (SAO) shock [17].
• More specifically, EITU failed to influence transcription of iNOS mRNA (Northern blot analysis), translation of iNOS protein (pulse experiments), or degradation of translated iNOS protein (pulse-chase experiments) [11].

References