Nicotine affects hydrogen sulfide concentrations in mouse kidney and heart but not in brain and liver tissues.

Nicotine, a potent parasympathomimetic alkaloid with stimulant effects, is contributing to addictive properties of tobacco smoking and is though used in the smoking cessation therapy. Hydrogen sulfide (H2S) is involved in physiology and pathophysiology of various systems in mammals. The interactions between nicotine and H2S are not fully recognized. The aim of the study is to assess the influence of nicotine on the H2S tissue concentrations in different mouse organs. Adult CBA male mice were administered intraperitoneally 1.5 mg/kg b.w. per day of nicotine (group D1, n = 10) or 3 mg/ kg b.w. per day of nicotine (group D2, n = 10). The control group (n = 10) received physiological saline. The measurements of the free and acid-labile H2S tissue concentrations were performed with the Siegel spectrophotometric modi ed method. ere was a significant increase in H2S concentrations in both nicotine doses groups in the kidney (D1 by 54.2%, D2 by 40.0%). In the heart the higher nicotine dose caused a marked decrease in H2S tissue level (by 65.4%), while the lower dose did not affect H2S content. Nicotine administration had no effect on H2S concentrations in the brain and liver. In conclusion, nicotine affects H2S tissue concentrations in kidney and heart but not in the liver and brain tissues.

Sodium Hydrosulfide Exerts a Transitional Attenuating Effect on Spermatozoa Migration in Vitro.

Hydrogen sulfide (H2S) has been shown to have a prominent role in the regulation of reproductive system function and fertility. The aim of the study was to assess the effect of a H2S donor, sodium hydrosulfide (NaHS), on mouse sperm migration in vitro. Special plates with 4 corner wells filled with balanced salt solution (control) and various NaHS solutions in concentrations of 2.5 mmol/l, 5 mmol/l or 10 mmol/l were applied. Spermatozoa from each male mouse were injected (the experiment was repeated with ten BALB/c 5-month old males) into the central pocket, connected with the wells with ducts. After 1 h, 2 h and 4 h of incubation, the number of spermatozoa in each well was determined using Bürker's counting chambers. The number ofspermatozoa in all corner wells were summed and the number of the cells in each well was treated as the percentage share of all the migrated spermatozoa. At the time points of 1 hour and 4 hours, no differences regarding chemotactic features of spermatozoa to the utilized solutions were observed. After two hours of incubation the attenuating effect of NaHS medium and high level solutions on spermatozoa migration was observed, but not for the low concentration mixture: H(3, N = 40) = 9.65, P = 0.022; control group vs 5 mmol/l NaHS solution: 36.0% vs 18.5%, P = 0.023; control group vs 10 mmol/l NaHS solution group: 36.0% vs 17.0%, P 0.011. In conclusion, NaHS has a transitional attenuating effect on spermatozoa migration in vitro.

Cocaine exposure alters H2S tissue concentrations in peripheral mouse organs.

BACKGROUND: Hydrogen sulfide (H2S) is well-known as a physiological mediator in the mammalian brain and peripheral tissues. Among several factors that change the concentration of H2S, oxidative stress and generation of reactive oxygen species, which accompany neurochemical actions of drugs of abuse, are of recent interest. OBJECTIVE: Limited data on the connection of cocaine and H2S levels prompted us to investigate the effect of this psychostimulant on the H2S concentration in the mouse brain and peripheral organs. METHODS: Male BALB/C mice were given several cocaine dosage and treatment regimens, and the free and acid-labile H2S tissue concentrations were determined with a modified spectrophotometric method of Siegel. RESULTS: We demonstrated the dose- and treatment-dependent decreases in the H2S level in the heart (83% of control level), and in the liver and kidney (17-34% of control levels) homogenates, but no changes were seen in the mouse brain. The strongest effect occurred after repeated administration of cocaine (20mg/kg) in all peripheral tissues. CONCLUSION: A reduction in the peripheral tissue H2S level in the heart, liver and kidney homogenates after repeated injections of cocaine may be the result of a strong toxic effect of the drug.

Metformin raises hydrogen sulfide tissue concentrations in various mouse organs.

BACKGROUND: The epidemic of diabetes mellitus type 2 forces to intensive work on the disease medication. Metformin, the most widely prescribed insulin sensitizer, exerts pleiotropic actions on different tissues by not fully recognized mechanisms. Hydrogen sulfide (H2S) is involved in physiology and pathophysiology of various systems in mammals and is perceived as a potential agent in the treatment of different disorders. The interaction between biguanides and H2S is unknown. The aim of the study is to assess the influence of metformin on the H2S tissue concentrations in different mouse organs. METHODS: Adult SJL female mice were administered intraperitoneally 100 mg/kg b.w. per day of metformin (group D1, n = 6) or 200 mg/kg b.w. per day of metformin (group D2, n = 7). The control group (n = 6) received physiological saline. The measurements of the free and acid-labile H2S tissue concentrations were performed with Siegel spectrophotometric modified method. RESULTS: There was a significant progressive increase in the H2S concentration along with the rising metformin doses as compared to the control group in the brain (D1 by 103.6%, D2 by 113.5%), in the heart (D1 by 11.7%, D2 by 27.5%) and in the kidney (D1 by 7.1%, D2 by 9.6%). In the liver, massive H2S accumulation was observed in the group D1 (increase by 420.4%), while in the D2 group only slight H2S level enhancement was noted (by 12.5%). CONCLUSION: Our experiment has shown that metformin administration is followed by H2S tissue concentrations increase in mouse brain, heart, kidney and liver.

Stevia, cyclamate and saccharin - natural and artificial sweeteners - exert no effect on sulfane levels in tissues.

The interactions among natural and artificial sweeteners and endogenous sulfur metabolism have never been investigated. CBA strain mice were administered orally stevia, cyclamate or saccharin in doses of 5 mg/kg of body weight in water solutions each. The measurements of the free and acid-labile sulfane (H2S) tissue concentrations in brain, heart, liver and kidney were performed with Siegel spectrophotometric modified method. No differences in comparisons between hydrogen sulfide concentrations in the control group and each sweetener group within every tissue type were noted. In conclusion, stevia, cyclamate and saccharine do not change the endogenous sulfur metabolism to the extent of causing sulfane tissue levels alterations.

Vitamin D3 (cholecalciferol) boosts hydrogen sulfide tissue concentrations in heart and other mouse organs.

Vitamin D3 is a crucial co-regulator of bone growth and remodeling, neuromuscular function, inflammation, proliferation, differentiation and apoptosis of cells. Intensive research on endogenous sulfur metabolism has revealed that hydrogen sulfide (H2S) is an important modulator of various physiological processes in mammals. Noteworthy, these compounds are perceived as potential agents in the treatment of numerous disorders, including cardiovascular diseases and different types of cancer. The interaction between vitamin D3 and H2S is unknown. The aim of the study is to assess the influence of cholecalciferol (vitamin D3, calcitriol) on H2S tissue concentrations in mouse brain, heart and kidney. Twenty four SJL mice were given intraperitoneal injections of cholecalciferol at 10000 IU/kg body weight (b.w.) per day (group A, n = 8) or 40000 IU/kg b.w. per day (group B, n = 8). The control group (n = 8) received physiological saline. Free H2S tissue concentrations were measured via the SIEGEL spectrophotometric modified method. There was a significant progressive increase in the H2S concentration along with the rising cholecalciferol doses as compared to the control group in the heart (by 29.6% and by 74.1%, respectively). Higher vitamin D3 dose caused H2S accumulation in the brain (by 10.9%) and in the kidney (by 10.1%). Our study has proven that cholecalciferol affects H2S tissue concentration in different mouse organs.

Carvedilol induces endogenous hydrogen sulfide tissue concentration changes in various mouse organs.

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 (H2S) is unknown. The aim of the study is to assess the influence of carvedilol on the H2S 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 H2S concentrations were performed according to the modified method of Siegel. A progressive decline in H2S 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 H2S tissue level in the heart - an increase by 75.5%. In the liver medium and high doses of carvedilol increased the H2S level by 48.1% and 11.8%, respectively. In the kidney, group D2 showed a significant decrease of H2S tissue level (22.5%), while in the D3 group the H2S concentration increased by 12.9%. Our study has proven that carvedilol affects H2S tissue concentration in different mouse organs.

Digoxin increases hydrogen sulfide concentrations in brain, heart and kidney tissues in mice.

The interest in digoxin has recently increased due to the expanding knowledge regarding endogenous cardiac glycosides and a potential oncological application of this drug. Hydrogen sulfide (H(2)S), a crucial co-modulator of various physiological processes, is involved in the pathophysiology of different disorders and may be useful in the treatment of some diseases. The interaction between cardiac glycosides and H(2)S is unknown. The aim of the study is to assess the influence of digoxin on H(2)S tissue concentrations in mouse brain, heart and kidney. Thirty male BALB/c mice were given intraperitoneal injections of digoxin at 0.5 mg/kg body weight (b.w.) per day (group D1, n = 10) or 1 mg/kg b.w. per day (group D2, n = 10). The control group (n = 10) received physiological saline. Free H(2)S tissue concentrations were measured via the Siegel spectrophotometric modified method. There was a significant, progressive increase in the H(2)S concentrations for both the low and high digoxin doses in the brain (7.7% and 8.5%, respectively), heart (by 6.0% and 22.1%, respectively) and kidney (by 7.6% and 13.0%, respectively). This report shows that digoxin administration is followed by an increase in the free H(2)S concentrations in mouse brain, heart and kidney tissues.

Paracetamol (acetaminophen) decreases hydrogen sulfide tissue concentration in brain but increases it in the heart, liver and kidney in mice.

The biological action ofN-acetyl-p-aminophenol - paracetamol (acetaminophen) has been demonstrated to involve different mechanisms and is still not clear. Hydrogen sulfide (H2S) has been shown to play an important role in many physiological and pathological processes including nociception. The interaction between acetaminophen and endogenous H2S 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 H2S concentration were performed with the Siegel spectrophotometric modified method. In the brain, the H2S tissue level decreased, but more significantly in the lower drug dose group. Conversely, there was a significant rise in the H2S 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 H2S concentration, increasing after administration of acetaminophen at 100 mg/kg. Our study demonstrates that paracetamol induces H2S tissue concentration changes in different mouse organs.

Atorvastatin affects the tissue concentration of hydrogen sulfide in mouse kidneys and other organs.

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.

Amlodipine affects endogenous hydrogen sulfide tissue concentrations in different mouse organs.

The interactions between calcium channel blockers' action and the endogenous hydrogen sulfide (H2S) biology are unknown. CBA strain mice were administered intraperitoneally 3 mg/kg b.w. per day or 10 mg/kg b.w. per day of amlodipine. The control group received physiological saline. The measurements of the free H2S tissue concentrations were performed with Siegel spectrophotometric modified method. There was as significant fall of H2S level in the brain and the liver in both groups. The lower amlodipine dose increased the H2S concentrations in the heart and kidneys while the higher one decreased H2S accumulation in those organs. Our experiment has shown that amlodipine interferes with H2S biology and affects its tissue concentrations in different mouse tissues.

Hypotensive effects of statins. A place for hydrogen sulfide in the puzzle?

Lipid lowering 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors--statins--significantly diminish the risk of cardiovascular morbidity and mortality in patients with cardiovascular diseases. Moreover, some clinical trials results indicate that this group of drugs reduces blood pressure, especially in patients with hypertension. In the article pleiotropic effects of statins that might have influence on blood pressure are discussed. Recent data on the role of gaseous messenger hydrogen sulfide (H2S) in cardiovascular biology and kidney physiology are presented with the focus on the latest findings of atorvastatin increasing H2S tissue concentration in kidneys.

Ramipril affects hydrogen sulfide generation in mouse liver and kidney.

Hydrogen sulfide (H2S) 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 H2S 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 H2S were performed using the modified spectrophotometric method of Siegel. There was a significant rise in the tissue concentration of H2S [microg/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 H2S 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.

Effects of aspirin on the levels of hydrogen sulfide and sulfane sulfur in mouse tissues.

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.

Ramipril enhances the endogenous hydrogen sulfide tissue concentration in mouse heart and brain.

BACKGROUND: Hydrogen sulfide (H2S) participates in regulation of different physiological and pathological processes of cardiovascular system and nervous system. The effect of ramipril - tissue specific angiotensin-converting enzyme inhibitor (ACEI) - exceeds renin-angiotensin aldosterone system (RAAS) blockade. The influence of ACEI on the metabolism of H2S remains obscure. The aim of the study is to assess the impact of ramipril administration on the tissue concentration of H2S in mouse heart and brain. METHOD: Thirty mice (CBA) of both sexes were given intraperitoneal injections of ramipril solution - 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). Control group received physiological saline in portions of the same volume - 0.2 ml. The measurements of the concentration of H2S were performed using spectrophotometric modified method of Siegel. RESULTS: There has been a significance rise in the tissue concentration of H2S [microg/g] in the heart in group D1 (4.91 +/- 0.07 vs 5.54 +/- 0.12; p = 0.005) and group D2 (4.91 +/- 0.07 vs 5.94 +/- 0.08; p < 0.001) and in the brain in group D1 (0.61 +/- 0.03 vs 0.69 +/- 0.02; p = 0.02) and non-significant increase in the brain D2 group (0.61 +/- 0.03 vs 0.65 +/- 0.03; p = 0.16). CONCLUSIONS: Ramipril enhances the concentration of endogenous H2S in mouse heart and brain.

Aspirin augments the concentration of endogenous hydrogen sulfide in mouse brain and liver.

Intraperitoneal injections of lysine acetylsalicylate (L-ASA, aspirin) in a dose of 10 mg during 5 consecutive days to BALB/c and B10.PL mice increased the concentration of endogenous hydrogen sulfide in their livers. The rise of hydrogen sulfur levels was shown also in brains of BALB/c females and B10.PL males, however in BALB/c male brains there is no statistically significant difference. The mechanism of aspirin action on H2S concentration is discussed.

Application of copper (II) in spectrophotometric determination of some drugs of aliphatic amine nature.

Anhydrous copper(II) acetate was applied to spectrophotometric determination of amitriptilline, doxepin and lignocaine in acetone solutions. The developed method was employed for determining these substances in pharmaceutical preparations. The obtained results has indicated both high precision and accuracy of the method.

Acidimetric titration of medicines being salts of weak acids and determining the end-point based on the iodate(V)-iodide reaction.

A sample being a salt of weak acid in a solvent is determined with hydrochloric acid in the presence of iodate, iodide and starch. The excess acid colours the solution blue.