Nephrotoxicity of sodium dichromate depending on the route of administration

Abstract

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.

Renal impairment caused by chronic occupational chromate exposure

“…Pathological studies have shown that signs of early nephropathy caused by Cr compounds were located in the proximal tubular brush border (Evan and Dail 1974;Franchini et al 1978;Kirschbaum et al 1981). Renal injury has been reported in both human and rodents after dichromate administration (Kim and Na 1991). Acute tubular necrosis and renal failure caused by massive absorption of chromic acid has also been reported (Berndt 1976;Pedersen and Mørch 1978;Appenroth and Bräunlich 1988).…”

The role of glutathione in the acute nephrotoxicity of sodium dichromate

“…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). Therefore, it seems that the inhibitory effect of Cr(VI) on mitochondrial respiration may not be the major cause of Cr(VI)-induced nephrotoxicity.…”

Effect of Potassium Dichromate on Properties and Biodegradation of Gum Arabic Based Bioplastic Membranes

“…Chromium compounds are used commercially in industrial welding, metal finishes, leather tanning, and wood preservation [15]. The chromium ion is considered as one of heavy metals that are very essential for biochemical and physiological functions in plants and animals [16]. Although chromium is an essential micronutrient for the growth of many organisms, but at high concentration it is toxic, carcinogenic and cause allergic [17,18,19,20].…”

“…Although chromium is an essential micronutrient for the growth of many organisms, but at high concentration it is toxic, carcinogenic and cause allergic [17,18,19,20]. Potassium dichromate has many harmful and toxic effects on mammals and rats [16]. For example, toxic effects of potassium dichromate on sex hormones of female albino rats [21], respiratory cancers [17,22], and ototoxicity that cause a wide range of fetal effects [23].…”