Acute toxic effect of sodium dichromate on metabolism

Kim, Eun; Na, Ki Jung

doi:10.1007/bf01974692

Cited by 14 publications

(4 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One might speculate that mitochondrial injury follows and results finally renal failure, because Cr(VI) irreversibly inhibits mitochondrial respiration in vitro (for review, see Rossi and Wetterhahn 1989). However, the toxic effects on cellular metabolism after Cr(VI) treatment of rats did not persist indefinitely, unlike the well-known metabolic inhibitors such as arsenic, cyanide, and mercury (Kim and Na 1990). In addition, metabolic disturbance has occurred with a lower dose (Kim and Na 1991 a) than the subthreshold doses of dichromate, which have been shown to have minimal effects on renal function (Christenson et al 1989).…”

Section: Discussionmentioning

confidence: 97%

“…metabolic disturbance, occurring only in the first 2 h after dichromate treatment Na 1990, 1991 a). Ascorbate pretreatment significantly decreased dichromate-induced metabolic disturbance, the indices of which were the early hyperglycemia and BUN elevation, accompanied by depletion of hepatic glycogen and decrease in serum total amino acids, respectively (Kim and Na 1990). Pretreatment with GSH, not taken up by liver cells, decreased dichromate-induced hyperglycemia; however, it had no effect on the BUN elevation induced by dichromate 2 h after treatment.…”

Section: Statisticsmentioning

confidence: 98%

See 1 more Smart Citation

The role of glutathione in the acute nephrotoxicity of sodium dichromate

Jeong

Lim

1992

Arch Toxicol

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Statisticsmentioning

confidence: 98%

The role of glutathione in the acute nephrotoxicity of sodium dichromate

Jeong

Lim

1992

Arch Toxicol

Self Cite

View full text Add to dashboard Cite

show abstract

“…Cr(VI) is readily taken up by cells (Berndt 1976;Wiegand et al 1985) and causes rapid metabolic disturbance (Kim and Na 1990); however, its nephrotoxic effects are not fully expressed at the initial time periods after treatment (Biber et al 1968;Hirsch 1973;Evan and Dail 1974). As shown in Fig.…”

Section: Discussionmentioning

confidence: 98%

Nephrotoxicity of sodium dichromate depending on the route of administration

Kim

1991

Arch Toxicol

Self Cite

View full text Add to dashboard Cite

A comparison of the effects of intraperitoneal and subcutaneous routes of administration of sodium dichromate on nephrotoxicity in rats was studied. Dichromate when injected subcutaneously (SC group) produced a higher degree of nephrotoxicity than when administered intraperitoneally (IP group). It caused severe progressive proteinuria followed by polyuria and glucosuria, reaching maximum levels at 3 days after treatment in the SC group, whereas it produced mild proteinuria without glucosuria in the IP group. The dose-dependent increases in blood urea nitrogen (BUN) and creatinine concentrations, shown in the SC group, were not observed in the IP group. However, between the two groups, there were no great differences in either the urinary excretion rate of chromium or the electrophoretic patterns of urinary protein in the day 1 urine specimens. Pretreatment of phenobarbital (PB) had no remarkable effect on the dichromate-induced nephrotoxicity. In contrast, it potentiated dichromate-induced hepatotoxicity, the indices of which were the elevation in serum alanine aminotransferase (ALT) activity and hepatic lipid peroxide formation. These results suggest that the dependence of dichromate-induced nephrotoxicity on the route of administration is related to the chemical forms of chromium reaching the kidney, and the necrotizing property of dichromate results from its metabolic fate in vivo.

show abstract

“…Rats were exposed via a single injection to 0.5, 1.25 and 2.5 mg/kg body weight (BW) CdCl 2 or 5, 10 and 20 mg/kg BW Na 2 Cr 2 O 7 . Previous studies have demonstrated the use of intraperitoneal injections of CdCl 2 [ 26 – 34 ] and Na 2 CrO 4 [ 35 – 38 ] in these dose ranges to induce tissue injury. Exposure times of 1, 3 and 7 days were chosen to investigate the acute effects of metal exposures and were based on previous investigations for changes in oxidative stress and recovery time [ 39 , 40 ].…”

Section: Methodsmentioning

confidence: 99%

Temporal Changes in Rat Liver Gene Expression after Acute Cadmium and Chromium Exposure

et al. 2015

View full text Add to dashboard Cite

U.S. Service Members and civilians are at risk of exposure to a variety of environmental health hazards throughout their normal duty activities and in industrial occupations. Metals are widely used in large quantities in a number of industrial processes and are a common environmental toxicant, which increases the possibility of being exposed at toxic levels. While metal toxicity has been widely studied, the exact mechanisms of toxicity remain unclear. In order to further elucidate these mechanisms and identify candidate biomarkers, rats were exposed via a single intraperitoneal injection to three concentrations of CdCl2 and Na2Cr2O7, with livers harvested at 1, 3, or 7 days after exposure. Cd and Cr accumulated in the liver at 1 day post exposure. Cd levels remained elevated over the length of the experiment, while Cr levels declined. Metal exposures induced ROS, including hydroxyl radical (•OH), resulting in DNA strand breaks and lipid peroxidation. Interestingly, ROS and cellular damage appeared to increase with time post-exposure in both metals, despite declines in Cr levels. Differentially expressed genes were identified via microarray analysis. Both metals perturbed gene expression in pathways related to oxidative stress, metabolism, DNA damage, cell cycle, and inflammatory response. This work provides insight into the temporal effects and mechanistic pathways involved in acute metal intoxication, leading to the identification of candidate biomarkers.

show abstract

Acute toxic effect of sodium dichromate on metabolism

Cited by 14 publications

References 19 publications

The role of glutathione in the acute nephrotoxicity of sodium dichromate

The role of glutathione in the acute nephrotoxicity of sodium dichromate

Nephrotoxicity of sodium dichromate depending on the route of administration

Temporal Changes in Rat Liver Gene Expression after Acute Cadmium and Chromium Exposure

Contact Info

Product

Resources

About