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In Vitro Studies on Degradation of Gamma-L-Glutamyl-L-Cysteine and Gamma-L-Glutamyl-D-Cysteine in Blood: Implications for Treatment of Stroke.

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Treatment for ischemic stroke involves a thrombolytic agent to re-establish blood flow in the brain. However, delayed reperfusion may cause injury to brain capillaries. Previous studies indicate that the antioxidant gamma-L-glutamyl-L-cysteine (γ-Glu-Cys) contributes to reducing reperfusion injury

Dietary S-allyl-L-cysteine reduces mortality with decreased incidence of stroke and behavioral changes in stroke-prone spontaneously hypertensive rats.

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S-Allyl-L-cysteine (SAC), an active organosulfur compound derived from garlic, was found to reduce mortality with lesser incidence of stroke and also to lower the overall stroke-related behavioral score in stroke-prone spontaneously hypertensive (SHRSP) rats by dietary administration. Consequently,

S-allyl L-cysteine diminishes cerebral ischemia-induced mitochondrial dysfunctions in hippocampus.

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Ischemic brain is highly vulnerable to free radicals mediated secondary neuronal damage especially mitochondrial dysfunctions. Present study investigated the neuroprotective effect of S-allyl L-cysteine (SAC), a water soluble compound from garlic, against cerebral ischemia/reperfusion (I/R)-induced

Protective effects of N-acetyl-L-cysteine in endotoxemia.

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Because oxygen free radicals have been implicated in the endothelial cell damage and in the myocardial depression occurring during severe sepsis, we investigated whether N-acetyl-L-cysteine (NAC) could influence the oxygen extraction capabilities during an acute reduction in blood flow induced by

Effects of N-acetyl-L-cysteine on regional blood flow during endotoxic shock.

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We previously reported that N-acetyl-L-cysteine (NAC), an oxygen free-radical scavenger, can increase the oxygen extraction capabilities during endotoxic shock when blood flow is progressively reduced. In the present study, we investigated whether the protective effects of NAC are related to an

Oxidation chemistry of (-)-norepinephrine in the presence of L-cysteine.

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The noradrenergic neurotransmitter (-)-norepinephrine (1) is very easily oxidized at physiological pH to an o-quinone (2) that normally cyclizes and subsequently oxidatively polymerizes to black melanin. In this investigation it is demonstrated that L-cysteine (CySH) can divert the melanin pathway

Neuroprotective mechanisms of S-allyl-L-cysteine in neurological disease.

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S-allyl-L-cysteine (SAC) is a sulfur-containing amino acid present in garlic and exhibits a wide range of biological activities such as antioxidant, anti-inflammatory, and anticancer agent. An earlier study demonstrated that SAC ameliorates oxidative damage in a model of experimental stroke.

N-acetyl-L-cysteine depresses cardiac performance in patients with septic shock.

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OBJECTIVE To investigate the effects of adjunctive therapy with parenteral N-acetyl-L-cysteine in patients with newly diagnosed septic shock. METHODS Prospective, randomized, double-blind, placebo-controlled study. METHODS Multidisciplinary intensive care unit at a university teaching

Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death

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A variety of pathogenic mechanisms, such as cytoplasmic calcium/zinc influx, reactive oxygen species production, and ionic imbalance, have been suggested to play a role in cerebral ischemia induced neurodegeneration. During the ischemic state that occurs after stroke or heart attack, it is observed

Role of mercury toxicity in hypertension, cardiovascular disease, and stroke.

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Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (N-acetyl-L-cysteine, alpha-lipoic acid, L-glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to

Long-lasting inhibition of presynaptic metabolism and neurotransmitter release by protein S-nitrosylation.

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Nitric oxide (NO) and related reactive nitrogen species (RNS) play a major role in the pathophysiology of stroke and other neurodegenerative diseases. One of the poorly understood consequences of stroke is a long-lasting inhibition of synaptic transmission. In this study, we tested the hypothesis

Sirt1-ROS-TRAF6 Signaling-Induced Pyroptosis Contributes to Early Injury in Ischemic Mice.

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Stroke is an acute cerebro-vascular disease with high incidence and poor prognosis, most commonly ischemic in nature. In recent years, increasing attention has been paid to inflammatory reactions as symptoms of a stroke. However, the role of inflammation in stroke and its underlying mechanisms

The metabolism and toxicity of hemin in astrocytes.

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Hemin is cytotoxic, and contributes to the brain damage that accompanies hemorrhagic stroke. In order to better understand the basis of hemin toxicity in astrocytes, the present study quantified hemin metabolism and compared it to the pattern of cell death. Heme oxygenase-1 (HO-1) expression was

Thresholds of ischemia salvageable with intravenous tissue plasminogen activator therapy: evaluation with cerebral blood flow single-photon emission computed tomographic measurements.

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OBJECTIVE This study investigated the cerebral blood flow (CBF) thresholds of ischemic cortices that were salvageable with intravenous tissue plasminogen activator (t-PA) infusion therapy. METHODS We retrospectively reviewed data for 20 patients who were treated with intravenous low-dose (7.2 mg)

Increased expression of ICAM-1 during reoxygenation in brain endothelial cells.

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OBJECTIVE Thrombolysis is a promising therapy for acute ischemic stroke. However, there is evidence that neutrophils may physically plug cerebral microvessels on reperfusion, preventing the full benefit of thrombolysis. We undertook this study to determine whether there was increased endothelial

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