Taurine protects against low-density lipoprotein-induced endothelial dysfunction by the DDAH/ADMA pathway

Tan, Binbin; Jiang, De-Jian; Huang, Huang; Jia, Sujie; Jiang, Jun-Lin; Hu, Chong; Li, Yuan‐Jian

doi:10.1016/j.vph.2006.11.006

Cited by 61 publications

(37 citation statements)

References 34 publications

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“…Moreover, the macrophages of taut Ϫ/Ϫ mice appear to change their stability in response to malaria, as circumstantially indicated by the increased systemic levels of TNF-␣ and IL-1␤, which are produced primarily by macrophages. This accords with other data showing, conversely, that taurine is able to dampen the effect of proinflammatory cytokines, including IL-1␤ (12) and TNF-␣ (10,24,33,34,44,47,60).…”

Section: Discussionsupporting

confidence: 92%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

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Deletion of the taurine transporter gene (taut) results in lowered levels of taurine, the most abundant amino acid in mammals. Here, we show that taut ؊/؊ mice have lost their ability to self-heal blood-stage infections with Plasmodium chabaudi malaria. All taut ؊/؊ mice succumb to infections during crisis, while about 90% of the control taut ؉/؉ mice survive. The latter retain unchanged taurine levels even at peak parasitemia. Deletion of taut, however, results in the lowering of circulating taurine levels from 540 to 264 mol/liter, and infections cause additional lowering to 192 mol/liter. Peak parasitemia levels in taut ؊/؊ mice are approximately 60% higher than those in taut ؉/؉ mice, an elevation that is associated with increased systemic tumor necrosis factor alpha (TNF-␣) and interleukin-1␤ (IL-1␤) levels, as well as with liver injuries. The latter manifest as increased systemic ammonia levels, a perturbed capacity to entrap injected particles, and increased expression of genes encoding TNF-␣, IL-1␤, IL-6, inducible nitric oxide synthase (iNOS), NF-B, and vitamin D receptor (VDR). Autopsy reveals multiorgan failure as the cause of death for malaria-infected taut ؊/؊ mice. Our data indicate that taut-controlled taurine homeostasis is essential for resistance to P. chabaudi malaria. Taurine deficiency due to taut deletion, however, impairs the eryptosis of P. chabaudi-parasitized erythrocytes and expedites increases in systemic TNF-␣, IL-1␤, and ammonia levels, presumably contributing to multiorgan failure in P. chabaudi-infected taut ؊/؊ mice.

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Section: Discussionsupporting

confidence: 92%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

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“…Hydrogen sulfide (H 2 S) is synthesized from 2 sulfur-containing amino acids, l-cysteine and l-methionine, by the 3 enzymes, cystathionine-γ-lyase (CSE), cystathionine-β-synthetase (CBS), and 3-mercaptopyruvate sulfurtransferase. 4 Taurine has several potentially beneficial cardiovascular effects that involve regulation of the nitric oxide system and endothelial function, 5,6 the renin-angiotensin-aldosterone system, 7,8 the oxidative stress system and sympathoadrenal activity, 9 and the endoplasmic reticulum stress system. 10,11 Epidemiological studies have demonstrated a reduction in plasma sulfur amino acids in hypertensive patients.…”

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confidence: 99%

Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension

et al. 2016

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P rehypertension is highly prevalent worldwide.1 It is estimated that ≈30% to 50% of the population have this condition. It frequently complicates other cardiometabolic risk factors and is closely associated with coronary heart disease, stroke, and renal dysfunction.2 Early intervention in prehypertension substantially prevents the incidence of hypertension and related damage to target organs. Currently, several strategies are used to treat prehypertension, including the incorporation of therapeutic lifestyle changes, such as healthy dietary intake and regular physical activity, as well as the use of antihypertensive drugs, such as an angiotensin II receptor blocker. Although these treatments improve prehypertension, poor compliance and limitations associated with antihypertensive medications prevent their application in the general population. Thus, there is an urgent need to identify reliable and accurate measures to prevent the development of prehypertension.Taurine (2-aminoethanesulfonic acid) is the most abundant, semiessential, sulfur-containing amino acid. It can be synthesized in vivo by cysteine in the presence of cysteine dioxygenase, 3 but taurine is mainly acquired from dietary sources, such as eggs, meat, and seafood. Hydrogen sulfide (H 2 S) is synthesized from 2 sulfur-containing amino acids, l-cysteine and l-methionine, by the 3 enzymes, cystathionine-γ-lyase (CSE), cystathionine-β-synthetase (CBS), and 3-mercaptopyruvate sulfurtransferase. 4 Taurine has several potentially beneficial cardiovascular effects that involve regulation of the nitric oxide system and endothelial function, 5,6 the renin-angiotensin-aldosteroneAbstract-Taurine, the most abundant, semiessential, sulfur-containing amino acid, is well known to lower blood pressure (BP) in hypertensive animal models. However, no rigorous clinical trial has validated whether this beneficial effect of taurine occurs in human hypertension or prehypertension, a key stage in the development of hypertension. In this randomized, double-blind, placebo-controlled study, we assessed the effects of taurine intervention on BP and vascular function in prehypertension. We randomly assigned 120 eligible prehypertensive individuals to receive either taurine supplementation (1.6 g per day) or a placebo for 12 weeks. Taurine supplementation significantly decreased the clinic and 24-hour ambulatory BPs, especially in those with high-normal BP. Mean clinic systolic BP reduction for taurine/placebo was 7.2/2.6 mm Hg, and diastolic BP was 4.7/1.3 mm Hg. Mean ambulatory systolic BP reduction for taurine/placebo was 3.8/0.3 mm Hg, and diastolic BP was 3.5/0.6 mm Hg. In addition, taurine supplementation significantly improved endothelium-dependent and endothelium-independent vasodilation and increased plasma H 2 S and taurine concentrations. Furthermore, changes in BP were negatively correlated with both the plasma H 2 S and taurine levels in taurine-treated prehypertensive individuals. To further elucidate the hypotensive mechanism, experimental studies were perfor...

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“…In the inflammation model we generated using LPS stimulation, both Arginine-ADMA and Arginine-NO pathways are found to be activated. On first sight, increase in both ADMA and nitrate/nitrite levels seem to be a contrary finding as it is known that ADMA is an endogenous inhibitor of NOS and increased levels of ADMA would decrease NO, thereby nitrate/nitrite levels [6,8,9]. However, in this model, it is obvious that NOS isoform catalysed NO synthesis is iNOS as endotoxin stimulates iNOS [20].…”

Section: Discussionmentioning

confidence: 84%

“…Endothelial dysfunction plays an important role in all stages of atherosclerotic diseases [5,7]. Asymmetric dimethylarginine (ADMA) is a L-arginine analog that functions as an endogenous inhibitor of all NOS isoforms and causes decreased NO levels [6,8,9]. ADMA is involved in the pathophysiology of human vascular diseases and considered to be not only a marker of endothelial dysfunction but also an important cardiovascular risk factor [6,10].…”

Section: Introductionmentioning

confidence: 99%