Physicochemistry of dinitrosyl iron complexes with thiolate ligands underlying their beneficial effect in endometriosis
Dinitrosyl iron complexes with thiolate ligands exert cytotoxic effects on endometrial tumors in rats with endometriosis by releasing NO and NO+ upon decomposition, similar to their proposed mechanism for inhibiting malignant tumor proliferation.
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The paper reviews the physicochemical basis of exogenous dinitrosyl iron complexes (DNIC) with thiolate ligands as donors of NO and NO+, describing how regulatory effects depend on higher-affinity transfer of NO/NO+ to heme- and thiol-containing biological targets. It argues that DNIC cytotoxicity arises from rapid DNIC decomposition in the presence of iron-chelating compounds, leading to high intracellular and tissue generation of NO and NO+. The authors specifically suggest that this cytotoxic mechanism underlies DNIC’s blocking effect on the development of benign endometrial tumors in rats with experimental endometriosis and may delay malignant tumor proliferation, while noting the general mechanistic nature of these proposals. This paper is centrally about endometriosis — it explains DNIC physicochemistry as the proposed mechanism for beneficial effects in experimental endometriosis models.
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References (29)
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