Ascorbic Acid in the Prevention of Chrome Dermatitis

Samitz, M. H.; Scheiner, D M; Katz, Sidney A.

doi:10.1080/00039896.1968.10665186

Cited by 18 publications

(6 citation statements)

References 5 publications

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“…The results presented demonstrate that there are great differences in the protective efficacy against dichromateinduced toxicity between ascorbate and GSH. Pretreatment with ascorbate, known as an antichrome agent (Samitz et al 1968), completely abolished both the metabolic disturbance and nephrotoxicity induced by dichromate (Figs 1, 2, and 3). In contrast, GSH pretreatment did not effectively decrease the toxicity of dichromate.…”

Section: Discussionmentioning

confidence: 88%

The role of glutathione in the acute nephrotoxicity of sodium dichromate

Jeong

Lim

1992

Arch Toxicol

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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.

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Section: Discussionmentioning

confidence: 88%

The role of glutathione in the acute nephrotoxicity of sodium dichromate

Jeong

Lim

1992

Arch Toxicol

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“…Recent studies 21 have shown that ascorbate accounted for ∼80% of the Cr(VI) reductase activity of rat liver and kidney ultrafiltrates, while no more than 20% could be attributed to sulfhydryl-containing factors, including GSH. Paradoxically, until recently, the reduction of Cr(VI) by AsA or ascorbate has drawn much less attention than it deserves compared with the Cr(VI)−GSH system, − probably because of the relative instability of the Cr(V)/ascorbate species under the studied conditions and the complexity of the redox processes. , As early as 1968, it was observed that AsA reduced Cr(VI) to Cr(III) with concomitant complex formation, but potential Cr(V) species produced in the reaction were not discussed . The reaction of Cr 2 O 7 2- with AsA was first studied using EPR spectrometry at pH values close to those of biological relevance, and these revealed the presence of relatively stable Cr(V) specieswith a t 1/2 for decomposition of ∼15 min .…”

Section: Introductionmentioning

confidence: 99%

EPR Spectroscopic Studies of the Reactions of Cr(VI) with l-Ascorbic Acid, l-Dehydroascorbic Acid, and 5,6-O-Isopropylidene-l-ascorbic Acid in Water.¹ Implications for Chromium(VI) Genotoxicity

and

Lay

1996

J. Am. Chem. Soc.

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The characterization of the Cr(V) intermediates in the reduction of Cr(VI) by l-ascorbic acid (l-AsA) in aqueous solution is described as a function of pH and ascorbate concentration. In the reaction of Cr(VI) with AsA at least seven EPR-active Cr(V) signals are present in addition to that of the ascorbate radical. The Cr(V)/ascorbate complex at g iso = 1.9791 (A iso = 16.4 × 10-4 cm-1) is much more stable in moderately acidic solution (pH 3−6) than in neutral and alkaline solutions. The reaction is affected by aerial O2 producing Cr(V)/ascorbate/peroxo complexes with signals at g iso = 1.9818 (A iso = 13.2 × 10-4 cm-1) and g iso = 1.9812 and another at g iso = 1.9824 (A iso = 12.9 × 10-4 cm-1). These signals are most prominent at near physiological pH values (7−8), and all were absent when the solutions were preincubated with catalase. The Cr(V)/ascorbate complex is most stabilized in a [AsA]:[Cr(VI)] ratio of 1:2, while the Cr(V)/ascorbate/peroxo complexes reach their maximum signal intensities at [AsA]:[Cr(VI)] = 1:1. None of these Cr(V) species are stable at pH > 10, and they are reduced rapidly to Cr(III) at [AsA]:[Cr(VI)] ratios above 2:1. This is the first characterization of such Cr(V)/ascorbate/peroxo complexes. They arise from the reduction of O2 during the aerial oxidation of AsA, and their identities were confirmed by studies on the reductions of Cr(VI) with AsA in the presence of H2O2. Their presence explains the O2 sensitivity of in vitro DNA damage, and implications for Cr(VI)-induced cancers are considered. The reductions of Cr(VI) by dehydroascorbic acid (DHAA) and 5,6-O-isopropylidene-l-ascorbic acid (i-p-AsA), in the presence and absence of H2O2 were also studied using EPR spectroscopy. From these studies, likely solution structures for the Cr(V) complexes formed in the reduction of Cr(VI) by AsA were assigned.

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“…In vitro studies have identified several cellular components that are capable of metabolizing chromium (Connett and Wetterhahn 1983). In general, only ascorbate and those molecules containing sulfhydryl groups are capable of easily reducing chromium(VI) at pH 7.4 (Samitz et al 1968;Wiegand et al 1984). In addition, cytochrome P-450 possesses chromate reductase activity (Gruber and Jennette 1978).…”

Section: Discussionmentioning

confidence: 99%

Acute toxic effect of sodium dichromate on metabolism

Kim

1990

Arch Toxicol

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The effect of sodium dichromate on cellular metabolism was investigated. Intraperitoneal injection of sodium dichromate into the rat (20 or 40 mg/kg) caused significant increases in serum lactate, pyruvate, and creatinine concentrations within 15 min after intoxication. Severe hyperglycemia occurred thereafter, as a result of increased hepatic glycogenolysis, which was seen in the first 2 h after dichromate. However, liver glycogen was resynthesized in 24 h-fasted rats after glucose refeeding. Dichromate decreased serum total amino acids, with a consequent increase in blood urea nitrogen (BUN) concentration. Unlike HgCl2 (2 mg/kg, i.p.), As2O3 (5 mg/kg, i.p.), and KCN (5 mg/kg, i.p.), dichromate showed the largest metabolic disturbance only in the early period after treatment. In addition, dichromate produced cyanosis, which appeared during the period of the accelerated glycolysis and breakdown of creatinine phosphate. Regardless of chemical species, only the hexavalent chromium compounds had an effect on the cellular metabolism. Trivalent chromium compounds had no effect at all. These results suggest that dichromate possesses a characteristic dual action on cellular metabolism, which might be related to its metabolic fate.

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Ascorbic Acid in the Prevention of Chrome Dermatitis

Cited by 18 publications

References 5 publications

The role of glutathione in the acute nephrotoxicity of sodium dichromate

The role of glutathione in the acute nephrotoxicity of sodium dichromate

EPR Spectroscopic Studies of the Reactions of Cr(VI) with l-Ascorbic Acid, l-Dehydroascorbic Acid, and 5,6-O-Isopropylidene-l-ascorbic Acid in Water.¹ Implications for Chromium(VI) Genotoxicity

Acute toxic effect of sodium dichromate on metabolism

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Ascorbic Acid in the Prevention of Chrome Dermatitis

Cited by 18 publications

References 5 publications

The role of glutathione in the acute nephrotoxicity of sodium dichromate

The role of glutathione in the acute nephrotoxicity of sodium dichromate

EPR Spectroscopic Studies of the Reactions of Cr(VI) with l-Ascorbic Acid, l-Dehydroascorbic Acid, and 5,6-O-Isopropylidene-l-ascorbic Acid in Water.1 Implications for Chromium(VI) Genotoxicity

Acute toxic effect of sodium dichromate on metabolism

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EPR Spectroscopic Studies of the Reactions of Cr(VI) with l-Ascorbic Acid, l-Dehydroascorbic Acid, and 5,6-O-Isopropylidene-l-ascorbic Acid in Water.¹ Implications for Chromium(VI) Genotoxicity