Our experiment has shown that metformin administration is followed by H2S tissue concentrations increase in mouse brain, heart, kidney and liver.

Hydrogen sulfide (H2S) is a crucial co-modulator of cardiovascular, nervous, digestive and excretory systems function. The pleiotropic action of atorvastatin exceeds simple 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibition and involves multiple biological mechanisms. This study assesses the influence of atorvastatin on the H2S tissue concentration in mouse brain, liver, heart and kidney. Twenty-four female CBA strain mice received an intraperitoneal injection. The mice were given one of the following solutions: 0.1 mg atorvastatin (5 mg/kg of body weight (b.w.)/day--group D1, n=8), 0.4 mg atorvastatin (20 mg/kg b.w./day--group D2, n=8) or a saline physiological control (0.2 ml--group C, n=8). A modified Siegel spectrophotometric method was used for the H2S tissue concentration measurements. There was a remarkable rise in the H2S concentration [μg/g] in the kidney (C: 5.26±0.09, D1: 5.77±0.11, p=0.0003; D2: 7.48±0.09, p<0.0001). There were also slight H2S tissue level changes in the brain (C: 1.61±0.01, D1: 1.75±0.03, p=0.0001; D2: 1.78±0.03, p<0.0001), the heart (C: 4.54±0.08, D1: 4.86±0.10, p=0.0027; D2: 4.56±0.07, p=0.6997) and the liver (C: 3.45±0.03, D1: 3.27±0.02, p=0.0001; D2: 3.31±0.02, p=0.0003). Our study supports the influence of atorvastatin on H2S tissue concentration in kidneys and other mouse organs.

Carvedilol induces endogenous hydrogen sulfide tissue concentration changes in various mouse organs. Folia biologica (Kraków) 59: 151-155. Carvedilol, a third generation non-selective adrenoreceptor blocker, is widely used in cardiology. Its action has been proven to reach beyond adrenergic antagonism and involves multiple biological mechanisms. The interaction between carvedilol and endogenous gasotransmitter hydrogen sulfide (H S) is unknown. The aim of the study is to assess the influence of carvedilol on the H S tissue level in mouse brain, liver, heart and kidney. Twenty eight SJL strain female mice were administered intraperitoneal injections of 2.5 mg/kg b.w./d (group D1, n = 7), 5 mg/kg b.w./d (group D2, n = 7) or 10 mg/kg b.w./d of carvedilol (group D3, n = 7). The control group (n = 7) received physiological saline in portions of the same volume (0.2 ml). Measurements of the free tissue H S concentrations were performed according to the modified method of Siegel. A progressive decline in H S tissue concentration along with an increase in carvedilol dose was observed in the brain (12.5%, 13.7% and 19.6%, respectively). Only the highest carvedilol dose induced a change in H S tissue level in the heart an increase by 75.5%. In the liver medium and high doses of carvedilol increased the H S level by 48.1% and 11.8%, respectively. In the kidney, group D2 showed a significant decrease of H S tissue level (22.5%), while in the D3 group the H S concentration increased by 12.9%. Our study has proven that carvedilol affects H S tissue concentration in different mouse organs.

The results of the present study suggest that ASA affects sulfur metabolism, in particular, renal and hepatic production of sulfane sulfur and NPSH in mice.

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