2015
DOI: 10.1039/c5ra00903k
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Catecholamine toxicity triggers myocardial membrane destabilization in rats: thymol and its counter action

Abstract: The present manuscript deals with the protective action of thymol against isoproterenol induced cardiotoxicity by reinstating ATPases and minerals as evidenced by decreased myocardial infarct size.

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Cited by 13 publications
(5 citation statements)
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“…Diminished concentrations of plasma GSH, an intracellular free-radical scavenger, is believed to be due to its counteractivity against free radicals in oxidative stress triggered by ISO [19]. Moreover, diminished levels of vitamin C and E are attributed to their increased utilization against reactive oxygen species (ROS) [20]. The increase in heart weight occurs due to a rise in edematous intramuscular space following cardiomyocyte injury and swelling, along with the invasion of the injured tissues by defensive inflammatory cells.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Diminished concentrations of plasma GSH, an intracellular free-radical scavenger, is believed to be due to its counteractivity against free radicals in oxidative stress triggered by ISO [19]. Moreover, diminished levels of vitamin C and E are attributed to their increased utilization against reactive oxygen species (ROS) [20]. The increase in heart weight occurs due to a rise in edematous intramuscular space following cardiomyocyte injury and swelling, along with the invasion of the injured tissues by defensive inflammatory cells.…”
Section: Discussionmentioning
confidence: 99%
“…In an in vitro assay, the reducing power of NKT was estimated using a previously described method of Oyaizu [53]. Varying volumes of NKT (10,20,30,40, and 50 µM) were mixed with 2.5 mL of phosphate buffer (0.2 M, pH 6.6) and 2.5 mL of potassium ferricyanide (1% w/v). The reaction mixture was incubated at 50 • C for 20 min.…”
Section: In Vitro Reducing Power Of Nktmentioning
confidence: 99%
“…As a counter mechanism against ROS, cells are packed with nonenzymatic antioxidants, such as glutathione and vitamin‐C. Many experimental, clinical, and epidemiologic studies have revealed that therapeutic intervention with antioxidants may interrupt the injury cascade and protect the myocardium at risk …”
Section: Introductionmentioning
confidence: 99%
“…The auto‐oxidation of catecholamines triggers the generation of highly cytotoxic free radicals that stimulates lipid peroxidation and causes irreversible damage to the myocardium . Thus, ISO‐induced MI is used as a common and well standardized experimental in vivo model to study the impact of many drug‐measuring cardiac function and biochemical changes with an extraordinary technical simplicity, low mortality, and reproducibility . The necrotic lesions developed via free radical–mediated oxidative stress after supramaximal doses of ISO also resemble MI in humans…”
Section: Introductionmentioning
confidence: 99%
“…Troponin elevation occurs through six pathobiological mechanisms: myocyte necrosis, apoptosis, normal myocyte turnover, cellular release of proteolytic troponin degradation products, increased cell wall permeability, and formation and release of membranous blebs 21) . Specifically, myocardial ischemia may induce apoptosis 22) , transient increases in cardiomyocyte permeability 23) , membranous blebs that rupture 24) , free radical overload 25) , increased troponin turnover 26) , and direct toxic effects of catecholamines 27) .…”
Section: Resultsmentioning
confidence: 99%