maleic acid/necroză

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Proximal tubular necrosis associated with maleic acid administration to the rat.

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Administration of maleic acid to the rat is used as an experimental model of Fanconi's syndrome. To determine the site and extent of morphologic injury within the kidney after maleic acid administration, we systematically examined renal tissue using light, transmission electron, and scanning

Nephrotoxicity of pravadoline maleate (WIN 48098-6) in dogs: evidence of maleic acid-induced acute tubular necrosis.

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Single oral administration of pravadoline maleate (WIN 48098-6), the maleic acid salt of WIN 48098, induced acute tubular necrosis (ATN) in male and female beagle dogs at dosages > or = 40 mg/kg (WIN 48098 base (31 mg/kg) and maleic acid (9 mg/kg)). Subsequent oral studies were conducted with

Tissue protective effect of xanthine oxidase inhibitor, polymer conjugate of (styrene-maleic acid copolymer) and (4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine), on hepatic ischemia-reperfusion injury.

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The detrimental role of superoxide anion (O(2)(-)) has been well documented in the pathogenesis of ischemia-reperfusion (I/R) injury. Our and other studies suggested that one critical source of O(2)(-) generation may be xanthine oxidase (XO). We thus hypothesized that I/R injury could be protected

Glutathione modulates rat and mouse hepatocyte sensitivity to tumor necrosis factor toxicity.

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OBJECTIVE Tumor necrosis factor (TNF)-alpha causes much of the hepatocellular injury and cell death that follows toxin-induced liver damage. The mechanism by which toxic liver injury sensitizes hepatocytes to TNF-alpha cytotoxicity is unknown. The aim of this study was to determine the role of the

Maleic acid dimethylester: evaluation of dermal toxicity and genotoxicity.

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Maleic acid dimethylester (MAD) was investigated in acute and subacute dermal toxicity studies, for sensitization potential, and for in vivo and in vitro genotoxicity. The acute dermal toxicity in rats was low (LD50 greater than 2000 mg/kg body weight). Only local effects, erythema and necrosis,

Total necrosis of hepatocellular carcinoma with a combination therapy of arterial infusion of chemotherapeutic lipiodol and transcatheter arterial embolization: report of 14 cases.

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Combination therapy consisting of Lipiodol (Laboratoire Guerbet, Villepinte, France) containing styrene maleic acid neocarzinostatin and transcatheter arterial embolization (L-TAE) has been an important conservative therapy for hepatocellular carcinoma (HCC). We examined the clinical and pathologic

Urinary loss of glucose, phosphate, and protein by diffusion into proximal straight tubules injured by D-serine and maleic acid.

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In several models of acute renal failure leakage of glomerular filtrate out of the tubule is an important pathogenetic mechanism; however, bidirectional diffusion of solute to account for certain pathophysiologic features of acute renal failure has received meager attention. Using micropuncture and

Pathophysiological effect of hepatic ischemia and reperfusion after hepatectomy in dogs with obstructive jaundice, focusing on the effect of coenzyme Q10 and styrene-co-maleic acid superoxide dismutase.

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The purpose of the present study was to elucidate the effect of hepatic reflow following ischemia on the remnant liver after hepatectomy with occluded hepatic blood inflow in dogs with obstructive jaundice. When 40% hepatectomy was performed with 10-min occlusion of hepatic blood inflow in dogs with

Styrene maleic acid-pirarubicin disrupts tumor microcirculation and enhances the permeability of colorectal liver metastases.

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BACKGROUND Doxorubicin is a commonly used chemotherapy limited by cardiotoxicity. Pirarubicin, derived from doxorubicin, selectively targets tumors when encapsulated in styrene maleic acid (SMA), forming the macromolecular SMA pirarubicin. Selective targeting is achieved because of the enhanced

In vitro and in vivo evaluation of tumor targeting styrene-maleic acid copolymer-pirarubicin micelles: Survival improvement and inhibition of liver metastases.

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Pirarubicin is a derivative of doxorubicin with improved intracellular uptake and reduced cardiotoxicity. We have prepared a micellar formulation of pirarubicin using styrene-maleic acid copolymer (SMA) of mean molecular weight of 1.2 kDa, which exhibits a mean diameter of 248 nm in solution. Being

Styrene-maleic acid copolymer-encapsulated CORM2, a water-soluble carbon monoxide (CO) donor with a constant CO-releasing property, exhibits therapeutic potential for inflammatory bowel disease.

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Carbon monoxide (CO), the physiological product of heme oxygenase during catabolic breakdown of heme, has versatile functions and fulfills major anti-oxidative and anti-apoptotic roles in cell systems. Administration of CO is thus thought to be a reasonable therapeutic approach in diseases-such as

Glutathione depletion enhances the formation of superoxide anion released into hepatic sinusoids after lipopolysaccharide challenge.

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BACKGROUND We examined the effects of glutathione depletion on the level of superoxide anion released into hepatic sinusoids after lipopolysaccharide challenge. METHODS Rats were given 1 mg/kg of maleic acid diethyl ester to deplete glutathione in vivo and then 0.5 mg/kg body weight of

Evaluation of the effects of subchronic oral administration of n-butyl maleate in Sprague-Dawley rats.

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n-Butyl maleate, also referred to as monobutyl maleate, is an ester of maleic acid, which is used as a counterion in the pharmaceutical industry. While substantial published data exist on short-term treatment, maleic acid-induced renal toxicity in the rat, no toxicity data are available on the

[Acute kidney insufficiency in the treatment of psoriasis using fumaric esters].

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We describe two patients who developed acute renal failure during therapy with fumaric acid-esters. Histologic findings after renal biopsy in one patient were compatible with the diagnosis of acute tubular necrosis (ATN), and renal function was restored after cessation of the medication. The

[Studies on the mechanisms of renal damages induced by nephrotoxic compounds].

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The present study was designed to evaluate the relationship between renal lipid peroxidation and acute renal damage induced by six nephrotoxic compounds: mercuric chloride (MC), glycerol (GL), maleic acid (MA), cephaloridine (CER), gentamicin (GM) and cisplatin (CDDP) in rats. Urine and blood

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