ascorbic-acid and sodium-bichromate

In order to attenuate or to prevent chromate-induced human erythrocytes injury, the influence of vitamin E, vitamin C, salicylate, deferoxamine, and N-ethylmaleimide on chromate-induced human erythrocytes haemoglobin oxidation and peroxidation were investigated. It was observed that pretreatment of human erythrocytes with vitamin E (20 microM), vitamin C (1 mM), salicylate (3 mM), and deferoxamine (4 mM) significantly increased (P=0.0001) chromate-induced human erythrocytes haemoglobin oxidation in a time dependent manner, while it was significantly decreased (P=0.0001) by pretreatment with N-ethylmaleimide (1 mM). In contrast, pretreatment of human erythrocytes with deferoxamine (4 mM) immediately inhibited (P=0.0001) chromate-induced human erythrocytes peroxidation, while it was significantly increased (P=0.0001) by pretreatment with N-ethylmaleimide (1 mM) during the first 4 h of cells exposition to chromate. For time periods superior to 6 h pretreatment with N-ethylmaleimide (1 mM) significantly decreased (P=0.0001) chromate-induced human erythrocytes peroxidation. It was concluded that care must be taken as these drugs are used to prevent against toxicity induced by chromium(VI) compounds.

Topics: Ascorbic Acid; Chromates; Deferoxamine; Erythrocytes; Ethylmaleimide; Hemoglobins; Humans; Oxidation-Reduction; Salicylates; Thiobarbituric Acid Reactive Substances; Time Factors; Vitamin E

Ascorbate treatment 30 min prior to sodium dichromate (20 or 30 mg/kg, s.c.) shows higher potency than that of glutathione (GSH) in protecting against both the metabolic disturbance and nephrotoxicity induced by dichromate. However, ascorbate treatment after 2 h of dichromate intoxication had no effect on dichromate-induced blood urea nitrogen (BUN) elevation 3 days after intoxication. In contrast, dichromate-induced glucosuria, which reached maximum levels at 3 days after treatment, was significantly decreased by GSH or N-acetyl cysteine (NAC) treatment, even if its administration was after 24 h of dichromate intoxication. Pretreatment with GSH depletors such as diethyl maleate (DEM) and buthionine sulfoximine (BSO) had no effect on dichromate-induced nephrotoxicity. GSH levels in the liver and kidney were not affected at 3 h after dichromate treatment. However, dichromate significantly increased tissue GSH levels with a marked increase in liver per kidney GSH ratio at 24 h after treatment, if food was withheld subsequent to dichromate treatment, indicating that GSH biosynthesis resulted from the accelerated protein breakdown. These results suggest that GSH-mediated dichromate reduction is not a kinetically favorable pathway in vivo; however, GSH plays an important role in protection against dichromate-induced nephrotoxicity. In addition, the cellular metabolism of dichromate in the early period after treatment is important in the pathogenesis of its nephrotoxicity.

Topics: Animals; Ascorbic Acid; Chromates; Glutathione; Kidney; Kidney Diseases; Male; Oxidation-Reduction; Rats; Rats, Sprague-Dawley; Sulfhydryl Compounds

Sodium dichromate ingestion in children is uncommon and potentially lethal. The most appropriate management is uncertain because of the lack of sound data contained in the few reports of successfully treated patients. Immediate treatment should include urgent induction of emesis, administration of ascorbic acid as an antidote, followed by supportive treatment.

Topics: Antidotes; Ascorbic Acid; Charcoal; Child, Preschool; Chromates; Emetics; Gastric Lavage; Humans; Male; Peritoneal Dialysis