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.

No abstract

This study was designed to investigate the effect of aspirin (ASA) on anaerobic cysteine metabolism, which yields sulfane sulfur-containing compounds and hydrogen sulfide (H(2)S), in mouse liver and brain. In order to solve this problem, we determined the levels of sulfane sulfur and H(2)S, and the activities of cystathionase, the enzyme directly engaged in H(2)S synthesis, and rhodanese, the enzyme that catalyzes sulfane sulfur transfer to different acceptors. Moreover, we examined the effect of ASA on glial Gomori-positive cells (GGPC) in the brain that contain sulfur-rich glial Gomori-positive material (GGPM). The studies indicated an ASA-induced decrease in H(2)S levels in the brain and an increase in the liver. ASA-treated animals had lower cerebral levels of GGPM-containing GGPCs but the sulfane sulfur level was not affected. Conversely, the sulfane sulfur content in the liver dropped. ASA did not change cystathionase and rhodanese activity in either organ. The obtained results revealed that ASA was able to influence anaerobic cysteine metabolism, leading to the formation of sulfane sulfur and H(2)S in the mouse liver and brain, and to affect the numbers of GGPM-containing GGPCs.

WILIÑSKI B., WILIÑSKI J., SOMOGYI E., GÓRALSKA M., PIOTROWSKA J. 2010. Ramipril affects hydrogen sulfide generation in mouse liver and kidney. Folia biol. (Kraków) 58: 177-180. Hydrogen sulfide (H S) is a modulator of various physiological and pathological processes in the cardiovascular and nervous system and plays an important role in the regulation of gastrointestinal tract, liver and kidney function. The effect of the pleiotropic action of the tissue specific angiotensin-converting enzyme inhibitor (ACEI), ramipril, exceeds renin-angiotensin aldosterone system (RAAS) blockade and involves different biological mechanisms. The aim of the study is to assess the influence of ramipril on H S production in mouse liver and kidneys. Thirty mice (CBA) of both sexes were given intraperitoneal injections of ramipril solutions 0.125 mg (5 mg/ kg group D1) and 0.25 mg (10 mg/ kg group D2) for 5 consecutive days at the same time of the day (10:30 am). The control group received physiological saline in portions of the same volume 0.2 ml. The measurements of the tissue concentration of H S were performed using the modified spectrophotometric method of Siegel. There was a significant rise in the tissue concentration of H S [Fg/g] in livers of group D1 (2.70 ± 0.02 vs 2.81 ± 0.06; P = 0.03) and group D2 (2.70 ± 0.02 vs 2.98 ± 0.03; P <0.001) and a significant decrease of H S kidney tissue concentration in group D1 (3.35 ±0.06 vs 3.15 ± 0.07; P = 0.02) and in group D2 (3.35 ± 0.06 vs 2.89 ± 0.03; P< 0.001).Our results show that ACEI ramipril affects hydrogen sulfide generation in mouse liver and kidneys.

acetaminophen) decreases hydrogen sulfide tissue concentration in brain but increases it in the heart, liver and kidney in mice. Folia biologica (Kraków) 59: 41-44.The biological action of N-acetyl-p-aminophenol -paracetamol (acetaminophen) has been demonstrated to involve different mechanisms and is still not clear. Hydrogen sulfide (H S) has been shown to play an important role in many physiological and pathological processes including nociception. The interaction between acetaminophen and endogenous H S is unknown. Twenty four female CBA strain mice were administered intraperitoneal injections of N-acetyl-p-aminophenol solution: paracetemol in doses of 30 mg/kg b.w. per day (group D1, n = 8) or 100 mg/kg b.w. per day (group D2, n = 8).. The control group (n = 8) received physiological saline in portions of the same volume 0.2 ml. The measurements of tissue H S concentration were performed with the Siegel spectrophotometric modified method. In the brain, the H S tissue level decreased, but more significantly in the lower drug dose group.Conversely, there was a significant rise in the H S tissue concentration in D1 and D2 groups in heart and kidney with the increase more pronounced in the group with the lower paracetamol dose. In the liver only the higher acetaminophen dose elicited a change in H S concentration, increasing after administration of acetaminophen at 100 mg/kg. Our study demonstrates that paracetamol induces H S tissue concentration changes in different mouse organs.