Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: Role of NF-κB, p38 and JNK MAPK pathway

Ghosh, Jyotirmoy; Das, Joydeep; Manna, Prasenjit; Sil, Parames C.

doi:10.1016/j.taap.2009.07.008

Cited by 160 publications

(93 citation statements)

References 33 publications

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“…This has been supported by other studies that associate its protective antioxidant properties with direct scavenging of free radicals and indirect preserving of membrane permeability (22,23). TA has therefore become a promising option to treat chemically induced illnesses (14,(24)(25)(26)(27). Recent investigations have shown that TA protects cells from the toxic effects of cadmium (Cd), paracetamol, and arsenic (As) that are mediated by free-radical attack (28)(29)(30)(31).…”

mentioning

confidence: 75%

The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human Lymphocytes

Türkez

Aydın

2012

Archives of Industrial Hygiene and Toxicology

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The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human LymphocytesPermethrin (PM) is a common pyrethroid pesticide used to control pests in agriculture, forestry, horticulture, health care, homes, and textile industry. It is confirmed as a strong mutagen in animals and humans. Taurine (TA) is an amino acid found in mammalian tissues that protects the cell against DNA damage. In this study, we investigated whether supplementation of human lymphocyte cultures with TA (in the concentrations of 25 μg mL-1, 50 μg mL-1and 100 μg mL-1) provided any protection against PM toxicity applied in the concentration of 200 μg mL-1. Genotoxicity was assessed using the micronucleus (MN) and sister chromatid exchanges (SCE) tests. In addition, we measured the total antioxidant capacity (TAC) and total oxidative stress (TOS) levels in the plasma to determine oxidative effects. PM increased SCE and MN levels and altered TAC and TOS levels. TA alone did not affect SCE and MN levels compared to controls, regardless of the concentration applied. In addition, it increased TAC levels without changing TOS levels. Moreover, it significantly buffered the negative cytogenetic and oxidative effects induced by PM in a clear dose-dependent manner. In conclusion, this study is the first to evidence the beneficial effects of TA against PM-induced DNA and oxidative damagesin vitro.

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mentioning

confidence: 75%

The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human Lymphocytes

Türkez

Aydın

2012

Archives of Industrial Hygiene and Toxicology

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“…MAPK , and JNK/SAPK (29,30). Activation of these pathways results in increased expression of numerous gene products that may cause cellular damage and play a major role in insulin resistance (31)(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Palmitate on Hepatic Insulin Resistance Are Mediated by NADPH Oxidase 3-derived Reactive Oxygen Species through JNK and p38MAPK Pathways

Gao

Nong

Huang

et al. 2010

Journal of Biological Chemistry

278

229

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Elevated plasma free fatty acid (FFA) levels in obesity may play a pathogenic role in the development of insulin resistance. However, molecular mechanisms linking FFA to insulin resistance remain poorly understood. Oxidative stress acts as a link between FFA and hepatic insulin resistance. NADPH oxidase 3 (NOX3)-derived reactive oxygen species (ROS) may mediate the effect of TNF-␣ on hepatocytes, in particular the drop in cellular glycogen content. In the present study, we define the critical role of NOX3-derived ROS in insulin resistance in db/db mice and HepG2 cells treated with palmitate. The db/db mice displayed increased serum FFA levels, excess generation of ROS, and upregulation of NOX3 expression, accompanied by increased lipid accumulation and impaired glycogen content in the liver. Similar results were obtained from palmitate-treated HepG2 cells. The exposure of palmitate elevated ROS production and NOX3 expression and, in turn, increased gluconeogenesis and reduced glycogen content in HepG2 cells. We found that palmitate induced hepatic insulin resistance through JNK and p38 MAPK pathways, which are rescued by siRNA-mediated NOX3 reduction. In conclusion, our data demonstrate a critical role of NOX3-derived ROS in palmitate-induced insulin resistance in hepatocytes, indicating that NOX3 is the predominant source of palmitate-induced ROS generation and that NOX3-derived ROS may drive palmitate-induced hepatic insulin resistance through JNK and p38 MAPK pathways.

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“…Excessive ROS production is directly deleterious by injuring DNA, proteins and lipids. It also favors cell death through activation of certain stress-sensitive signaling pathways, such as nuclear factor κB, p38MAPK, and c-Jun N-terminal kinase (JNK) [51,52] . In addition, a general cellular oxidative stress inevitably affects the intricate redox homeostasis in the ER lumen [53][54][55] .…”

Section: Lipotoxic Oxidative Stressmentioning

confidence: 99%

Lipotoxicity in the liver

Zámbó

Simon-Szabó

Szelényi

et al. 2013

WJH

157

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Obesity due to excessive food intake and the lack of physical activity is becoming one of the most serious public health problems of the 21 st century. With the increasing prevalence of obesity, non-alcoholic fatty liver disease is also emerging as a pandemic. While previously this pathophysiological condition was mainly attributed to triglyceride accumulation in hepatocytes, recent data show that the development of oxidative stress, lipid peroxidation, cell death, inflammation and fibrosis are mostly due to accumulation of fatty acids, and the altered composition of membrane phospholipids. In fact, triglyceride accumulation might play a protective role, and the higher toxicity of saturated or trans fatty acids seems to be the consequence of a blockade in triglyceride synthesis. Increased membrane saturation can profoundly disturb cellular homeostasis by impairing the function of membrane receptors, channels and transporters. However, it also induces endoplasmic reticulum stress via novel sensing mechanisms of the organelle's stress receptors. The triggered signaling pathways in turn largely contribute to the development of insulin resistance and apoptosis. These findings have substantiated the lipotoxic liver injury hypothesis for the pathomechanism of hepatosteatosis. This minireview focuses on the metabolic and redox aspects of lipotoxicity and lipoapoptosis, with special regards on the involvement of endoplasmic reticulum stress responses. Key words: Saturated fatty acid; Lipotoxicity; Steatosis; Lipoapoptosis; Endoplasmic reticulum stress Core tip: Surplus of free fatty acids contributes to hepatic injuries in obesity and type 2 diabetes. Intracellular accumulation of fatty acyl-CoA causes oxidative and endoplasmic reticulum (ER) stress, which lead to cell death, inflammation and fibrosis. Steatohepatosis is the consequence of an intensive fat synthesis, aiming to reduce the metabolic burden. The higher toxicity of saturated vs unsaturated fatty acids is partly due to a limited capacity of the liver cells to insert them into triglycerides. Moreover, increased membrane saturation triggers the ER stress response though a unique mechanism, which aggravates the metabolic derangements and liver injuries.

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Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: Role of NF-κB, p38 and JNK MAPK pathway

Cited by 160 publications

References 33 publications

The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human Lymphocytes

The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human Lymphocytes

The Effects of Palmitate on Hepatic Insulin Resistance Are Mediated by NADPH Oxidase 3-derived Reactive Oxygen Species through JNK and p38MAPK Pathways

Lipotoxicity in the liver

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