Abstract:H2S has a key role in vascular homeostasis during physiology and in pathological states. H2S-based therapies may have a role in several vascular diseases.
“…Hydrogen sulphide-based therapies have therapeutic potential in diseases such as renal ischemia-reperfusion disorders, hypertension, and hypertensive-associated heart disease. Thus, several compounds releasing H 2 S have been described as candidates for the treatment of vascular disease [30] and decreasing platelet-leukocyte aggregation and improving endogenous thrombolysis [31]. Hydrogen sulphide and oestrogen have been shown to inhibit the development of atherosclerosis [32] through upregulating protein S-nitrosylation [33].…”
Section: Hydrogen Sulphide and Body Physiologymentioning
Sulphurous mineral waters have been traditionally used in medical hydrology as treatment for skin, respiratory, and musculoskeletal disorders. However, driven by recent intense research efforts, topical treatments are starting to show benefits for pulmonary hypertension, arterial hypertension, atherosclerosis, ischemia-reperfusion injury, heart failure, peptic ulcer, and acute and chronic inflammatory diseases. The beneficial effects of sulphurous mineral waters, sulphurous mud, or peloids made from sulphurous mineral water have been attributed to the presence of sulphur mainly in the form of hydrogen sulphide. This form is largely available in conditions of low pH when oxygen concentrations are also low. In the organism, small amounts of hydrogen sulphide are produced by some cells where they have numerous biological signalling functions. While high levels of hydrogen sulphide are extremely toxic, enzymes in the body are capable of detoxifying it by oxidation to harmless sulphate. Hence, low levels of hydrogen sulphide may be tolerated indefinitely. In this paper, we review the chemistry and actions of hydrogen sulphide in sulphurous mineral waters and its natural role in body physiology. This is followed by an update of available data on the impacts of exogenous hydrogen sulphide on the skin and internal cells and organs including new therapeutic possibilities of sulphurous mineral waters and their peloids.
“…Hydrogen sulphide-based therapies have therapeutic potential in diseases such as renal ischemia-reperfusion disorders, hypertension, and hypertensive-associated heart disease. Thus, several compounds releasing H 2 S have been described as candidates for the treatment of vascular disease [30] and decreasing platelet-leukocyte aggregation and improving endogenous thrombolysis [31]. Hydrogen sulphide and oestrogen have been shown to inhibit the development of atherosclerosis [32] through upregulating protein S-nitrosylation [33].…”
Section: Hydrogen Sulphide and Body Physiologymentioning
Sulphurous mineral waters have been traditionally used in medical hydrology as treatment for skin, respiratory, and musculoskeletal disorders. However, driven by recent intense research efforts, topical treatments are starting to show benefits for pulmonary hypertension, arterial hypertension, atherosclerosis, ischemia-reperfusion injury, heart failure, peptic ulcer, and acute and chronic inflammatory diseases. The beneficial effects of sulphurous mineral waters, sulphurous mud, or peloids made from sulphurous mineral water have been attributed to the presence of sulphur mainly in the form of hydrogen sulphide. This form is largely available in conditions of low pH when oxygen concentrations are also low. In the organism, small amounts of hydrogen sulphide are produced by some cells where they have numerous biological signalling functions. While high levels of hydrogen sulphide are extremely toxic, enzymes in the body are capable of detoxifying it by oxidation to harmless sulphate. Hence, low levels of hydrogen sulphide may be tolerated indefinitely. In this paper, we review the chemistry and actions of hydrogen sulphide in sulphurous mineral waters and its natural role in body physiology. This is followed by an update of available data on the impacts of exogenous hydrogen sulphide on the skin and internal cells and organs including new therapeutic possibilities of sulphurous mineral waters and their peloids.
“…Dysregulation of the hydrogen sulfide (H 2 S) pathway has been suggested to contribute to the underlying mechanisms of PE and FGR. H 2 S contains pro-angiogenic, anti-inflammatory, vasodilatory, and antioxidant properties, and thus is important in vascular adaptation [8][9][10]. This gasotransmitter is endogenously produced in the placenta from L-cysteine by enzymes including cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) [11].…”
Aberrant production of hydrogen sulfide (H2S) has been linked to preeclampsia. We hypothesized that sodium thiosulfate (STS), a H2S donor, reduces hypertension and proteinuria, and diminishes fetal growth restriction in the Dahl salt-sensitive (S) rat, a spontaneous model of superimposed preeclampsia. In addition to a control group (n = 13), two groups received STS via drinking water at a dose of 2 g (n = 9) or 3 g per kg body weight per day (n = 8) from gestational day (GD) 10 to 20. Uterine artery resistance index was measured (GD18), urinary protein excretion rate was determined (GD19), and blood pressure and fetal outcomes were evaluated (GD20). At 2 g, STS had no effect on preeclamptic symptoms or fetal outcome. At 3 g, STS reduced maternal hypertension (121.8 ± 3.0 vs. 136.3 ± 2.9), but increased proteinuria (89 ± 15 vs. 56 ± 5 mg/24 h), and relative kidney weight (0.86 ± 0.04 vs. 0.73 ± 0.02%). Fetal/placental weight ratio was reduced (3.83 ± 0.07 vs. 4.31 ± 0.08) without affecting litter size. No differences in uterine artery flow or renal histological damage were noted across treatment groups. While these data suggest a promising antihypertensive effect that could imply prolongation of preeclamptic pregnancies, the unfavorable effects on proteinuria, kidney weight, and fetal/placental weight ratio implies that clinical implementation of STS is contra-indicated until safety for mother and child can be verified.
“…42 The authors posited that in preeclampsia, attenuation of placental growth factor-induced EDH contributes to impaired function of resistance arteries and leads to maternal hypertension. 42 Recent studies suggest the involvement of hydrogen sulfide, a gaseous signaling molecule that induces EDH, 43 in preeclampsia-associated vascular dysfunction. Circulating hydrogen sulfide is reduced in pregnant women with preeclampsia, 44 and expression of cystathionine-β-synthase, the enzyme that is involved in desulfuration of l-cysteine into hydrogen sulfide, is attenuated in endothelial cells stimulated with plasma from pregnancies with preeclampsia.…”
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