Liver necrosis and fulminant hepatic failure in rats: protection by oxyanionic form of tungsten

Pawa, Sonica; Ali, Shakir

doi:10.1016/j.bbadis.2003.12.004

Cited by 50 publications

(33 citation statements)

References 42 publications

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“…TAA generates liver damage by upregulating hepatic XO activity [2]. This feature of TAA makes it a proper hepatotoxic agent for testing the effects of XO inhibition [3]. Therefore inhibition of XO may be a logical approach for prevention of tissue damage resulting from XO-derived ROS.…”

Section: Discussionmentioning

confidence: 99%

“…Despite technological advances and improvement in intensive care conditions, ALF continues to be one of the most challenging problems in clinical practice [1]. In various liver injury models [2][3][4][5], it has been revealed that increased xanthine oxidase (XO) activity plays pivotal role in the oxidative stress-induced hepatic damage. XO is widely distributed throughout various tissues with the highest level in the liver [6,7].…”

Section: Introductionmentioning

confidence: 99%

“…XO-derived oxidative stress-induced tissue damage may develop in various ways such as DNA damage by reactive oxygen species (ROS) [2], activation of NF-κB signaling pathway, and severe inflammatory cell infiltration [8]. Thioacetamide (TAA) has also been demonstrated to cause liver injury by increased XO-derived ROS formation [3,7].…”

Section: Introductionmentioning

confidence: 99%

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Allopurinol Ameliorates Thioacetamide-Induced Acute Liver Failure by Regulating Cellular Redox-Sensitive Transcription Factors in Rats

et al. 2012

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Oxidative stress plays important role in the development of acute liver failure. In this study, we investigated effects of allopurinol (AP) upon thioacetamide (TAA)-induced liver injury and the potential mechanisms leading to amelioration in inflammation with AP treatment. Acute liver failure was induced by intraperitoneal administration of TAA (300 mg/kg/day for 2 days). Thirty-five rats were divided into five groups as control (group 1), TAA (group 2), TAA + 25AP (group 3), TAA + 50 AP (group 4), and TAA + 100AP (group 5). The number of animals in each group was seven. At the end of the study, histopathological, biochemical, and western blot analysis were done. TAA treatment significantly increased serum levels of aminotransferases, liver malondialdehyde (MDA), nuclear factor-kappa B (NF-қB ), activator protein-1 (AP-1), tumor necrosis factor-alpha (TNF-α), cyclooxygenase-2 (COX-2) and interleukin-6 (IL-6) levels, and the necro-inflammation scores. Nevertheless, nuclear factor E2-related factor-2 and heme oxygenase-1 (HO-1) expressions in the liver were decreased by TAA. AP treatment significantly lowered the serum levels of aminotransferases (P < 0.01) and liver MDA, NF-κB, AP-1, TNF-α, COX-2, and IL-6 expressions (P < 0.05). Moreover, AP restored the liver Nrf2 and HO-1 expressions and improved the necro-inflammation scores significantly. AP improves oxidative stress-induced liver damage by regulating cellular redox-sensitive transcriptor factors and expression of pro-inflammatory and antioxidant defense mechanisms. AP probably exerts these beneficiary features by its free radical scavenging ability in a dose-dependent manner.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Allopurinol Ameliorates Thioacetamide-Induced Acute Liver Failure by Regulating Cellular Redox-Sensitive Transcription Factors in Rats

et al. 2012

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“…27,28) Many studies demonstrated that tungstate has effects on the anti-diabetes, 29,30) hepatoprotection, 22,31) and various beneficial actions.…”

mentioning

confidence: 99%

“…27,28) Many studies demonstrated that tungstate has effects on the anti-diabetes, 29,30) hepatoprotection, 22,31) and various beneficial actions. 32,33) Furthermore, it was well known that XO activity was decreased by tungstate via replacement of molybdenum in enzyme molecule.…”

mentioning

confidence: 99%

The Effects of Tungstate on Skin Lesions Caused by PPD in Rats

Lee¹,

Cho

S³

2008

Biological & Pharmaceutical Bulletin

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Red brownish p-phenylenediamine (PPD) has been widely used as one of the ingredients in hair dyes. The use by consumers of hair dye results in exposure of the hair, scalp skin, eyes, nail, and hands to PPD. PPD studies have found that women using dye with a formulation that included PPD suffered acute sensitive responses such as headaches, dizziness, and systemic anaphylaxis for the long time after using the product.1) And in patch tests, PPD caused erythema, rash, and a burning sensation on human skin. Furthermore, workers occupationally exposed to PPD in the field suffered from the bladder cancer.2,3) Previous studies have shown that PPD application induces injury to rat skin. 4,5) It is reported that PPD is metabolized to N-acetylated adducts as the major metabolites by N-acetyltransferase in human skin and liver, 6) and rats. 7) Moreover, it is reported that N-oxidation of arylamines like PPD occurs in the liver and is generally considered to involve cytochrome P450. 8) Furthermore, N-acetylated PPD metabolites are less toxic and they are excreted in urine.9) And, lipid peroxidation was increased while glutathione was decreased in skin by PPD application.5,10) In addition, PPD toxicity is increased by MnSOD polymorphism 11) while PPD toxicity is alleviated by thiol antioxidants.12) These reports suggest that production of ROS can be related to PPD skin toxicity. However, there are ongoing controversies whether PPD induced organ toxicity or whether it is safe in animal and clinical experiment. 13,14) It is well known that xenobiotic-induced tissue damage is related to reactive metabolites as well as produced reactive oxygen species (ROS) such as superoxide, hydroxyl radical, single oxygen and hydrogen peroxide under the metabolism. 15,16) Many studies have reported an imbalance between ROS generating systems and scavenging systems such as the increasing of ROS generating enzymes and/or decreasing of scavenging enzymes and nonenzymatic antioxidants. 17,18) It is accepted that xanthine oxidase (XO), one of the ROS generating systems, is increased in the injured cells.19) It has been revealed that inhibition of XO activity by allopurinol 20) or tungstate 21) alleviates experimental tissue damage. This indicates therefore a relationship of XO to skin cell injury, which suggests that the XO plays a role in the toxicity by the exposure of xenobiotics such as cosmetics and chemicals due to relatively higher XO activity in skin tissue compared with other tissues except liver and intestine. 19,22) It is reported that oxidized PPD, imine derivatives by hydrogen peroxide 23) could induce malignant and benign tumors in the mammary gland, uterus, and soft tissues of rats.24) Moreover, it is reported that XO could generate ROS such as superoxide and hydrogen peroxide.25,26) So, we hypothesized hydrogen peroxide derived from the XO system in skin involved with PPD oxidation and produced oxidized PPD is associated with dermal tissue damage.It is well established that sodium tungstate has relatively lower toxicity than that o...

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High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria

Cheraghi

Hajiabedi

Niaghi

et al. 2018

J Biochem & Molecular Tox

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Tungstate (W) is recognized as an agent of environmental pollution and a substitute to depleted uranium. According to some preliminary studies, tungstate toxicity is related to the formation of reactive oxygen species (ROS) under abnormal pathological conditions. The kidneys and liver are the main tungstate accumulation sites and important targets of tungstate toxicity. Since the mitochondrion is the main ROS production site, we evaluated the mechanistic toxicity of tungstate in isolated mitochondria for the first time, following a two‐step ultracentrifugation method. Our findings demonstrated that tungstate‐induced mitochondrial dysfunction is related to the increased formation of ROS, lipid peroxidation, and potential membrane collapse, correlated with the amelioration of adenosine triphosphate and glutathione contents. The present study indicated that mitochondrial dysfunction was associated with disruptive effects on the mitochondrial respiratory chain and opening of mitochondrial permeability transition (MPT) pores, which is correlated with cytochrome c release. Our findings suggest that high concentrations of tungstate (2 mM)‐favored MPT pore opening in the inner membranes of liver and kidney mitochondria of rats. Besides, the results indicated higher tungstate susceptibility in the kidneys, compared with the liver.

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Liver necrosis and fulminant hepatic failure in rats: protection by oxyanionic form of tungsten

Cited by 50 publications

References 42 publications

Allopurinol Ameliorates Thioacetamide-Induced Acute Liver Failure by Regulating Cellular Redox-Sensitive Transcription Factors in Rats

Allopurinol Ameliorates Thioacetamide-Induced Acute Liver Failure by Regulating Cellular Redox-Sensitive Transcription Factors in Rats

The Effects of Tungstate on Skin Lesions Caused by PPD in Rats

High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria

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