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Acetone effects on N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity.

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Acetone has been shown to potentiate the toxicity of many halogenated hydrocarbons. The purpose of this study was to determine if acetone could alter the acute nephrotoxicity produced by the experimental fungicide N-(3,5-dichlorophenyl)succinimide (NDPS). Male Fischer 344 rats were administered

Urinary enzyme excretion as a parameter for detection of acute renal damage mediated by N-(3,5-dichlorophenyl)succinimide (NDPS) in Fischer 344 rats.

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The kidney has been identified as the specific target organ for in vivo exposure to an agricultural fungicide, N-(3,5-dichlorophenyl)succinimide (NDPS). The goal of this study was to determine if urinary protein and enzyme excretion were sensitive, non-invasive markers for NDPS-induced renal damage.

Acute nephrotoxicity of N-phenyl and N-(monochlorophenyl) succinimides in Fischer 344 and Sprague-Dawley rats.

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The experimental fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) has been shown to be nephrotoxic in Sprague-Dawley and Fischer 344 rats. The purpose of this study was to evaluate the role of the chlorine atoms in NDPS-induced nephropathy. Male Sprague-Dawley or Fischer 344 rats received a single

The effect of probenecid on acute N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in the Fischer 344 rat.

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N-(3,5-Dichlorophenyl)succinimide (NDPS), an experimental agricultural fungicide, has been shown to produce selective nephrotoxicity in rats. Previous studies have shown that a metabolite(s) of extrarenal origin contributes to acute NDPS-induced nephrotoxicity. The purpose of this study was to

Role of chloride groups in the nephrotoxic potential of N-(3,5-dichlorophenyl)-2-hydroxysuccinimide, an oxidative metabolite of N-(3,5-dichlorophenyl)succinimide.

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Although the addition of chloride groups to the phenyl ring of N-phenylsuccinimide (NPS) is known to enhance the nephrotoxic potential of NPS, the mechanism of this enhancement is unknown. One chlorinated NPS derivative, N-(3,5-dichlorophenyl)succinimide (NDPS), is a potent nephrotoxicant which

Effect of calcium antagonism by nifedipine and chlorpromazine on acute N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in Fischer 344 rats.

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The nephrotoxicity induced by a wide variety of chemical compounds can be attenuated by agents which modify calcium ion (Ca2+) movement across membranes or calcium-dependent processes. The purpose of this study was to examine the ability of nifedipine, a calcium channel blocking drug, and

Nephrotoxicity of N-(3,5-dichlorophenyl)succinimide metabolites in vivo and in vitro.

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The experimental fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) has been shown to produce selective nephrotoxicity at least in part through the actions of one or more metabolites. The purpose of this study was to (1) determine the nephrotoxic potential of three known NDPS metabolites;

Nephrotoxicity of N-(3-bromophenyl)-2-hydroxysuccinimide: role of halogen groups in the nephrotoxic potential of N-(halophenyl) succinimides.

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Among N-(halophenyl)succinimides. N-(3,5-dichlorophenyl)succinimide (NDPS) is a potent nephrotoxicant as well as an agricultural fungicide. Although two chloride groups on the phenyl ring are essential to induce optimal nephrotoxicity, the role of halogen groups in NDPS nephrotoxicity is not clear.

Buthionine sulfoximine (BSO) and N-(3,5-dichlorophenyl)succinimide nephrotoxicity: temporal aspects of BSO administration and BSO effects on renal transport systems.

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The agricultural fungicide, N-(3,5-dichlorophenyl)succinimide (NDPS) induces acute polyuric renal failure which is attenuated by pretreatment with the glutathione depletors, diethyl maleate or buthionine sulfoximine (BSO). In the present study, the temporal aspects of BSO attenuation of NDPS

Effect of dimethyl sulfoxide on N-(3,5-dichlorophenyl)succinimide (NDPS) and NDPS metabolite nephrotoxicity.

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Dimethyl sulfoxide (DMSO) is frequently used as a solvent to assist in dissolving compounds which are not readily soluble in other injection vehicles. The purpose of this study was to determine the suitability of DMSO as a vehicle for administering the nephrotoxicant,

Acute effects of the antiepileptic succinimides on the urinary tract and potentiation of phensuximide-induced urotoxicity by phenobarbital.

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Phensuximide (PSX), methsuximide (MSX) and ethosuximide (ESX) are succinimide antiepileptic agents used worldwide in the treatment of absence seizures. A previous study from our laboratory demonstrated that PSX (0.3 or 0.6 mmol kg-1 day-1, i.p.) induced urotoxicity following daily administration for

Role of glutathione in acute N-(3,5-dichlorophenyl) succinimide-induced nephrotoxicity in Sprague-Dawley and Fischer 344 rats.

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N-(3,5-Dichlorophenyl)succinimide (NDPS), an experimental agricultural fungicide, has been shown to be a selective nephrotoxin in Sprague-Dawley and Fischer 344 rats. Previous studies have demonstrated that a toxic metabolite contributes to or is responsible for acute NDPS-induced nephrotoxicity.

N-(3,5-Dichlorophenyl)succinimide nephrotoxicity in the Fischer-344 rat.

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The nephrotoxic potential of N-(3,5-dichlorophenyl)succinimide (NDPS) was examined, in male Fischer-344 rats. Rats were administered NDPS (0.1, 0.2, 0.4 or 1.0 mmol/kg intraperitoneally (i.p.) or sesame oil (2.5 ml/kg, i.p.), and renal function was monitored at 24 and 48 h. NDPS (0.1 mmol/kg)

Effect of succinimide ring modification on N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in Sprague-Dawley and Fischer 344 rats.

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N-(3,5-Dichlorophenyl)succinimide (NDPS) has proven to be an effective experimental agricultural fungicide. However, NDPS produces marked nephrotoxicity in Sprague-Dawley and Fischer 344 rats. The purpose of this study was to determine the importance of an intact, unsubstituted succinimide ring for

Effect of buthionine sulfoximine on acute N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in Fischer 344 rats.

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The experimental agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) has been shown to be a nephrotoxicant in Fischer 344 rats. Results of a previous study conducted in our laboratory suggested that glutathione might be an important modulator of NDPS-induced nephrotoxicity. The purpose

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