TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

CHROMIUM 2282. HEALTH EFFECTS1986a, 1986b; Montaldi et al. 1987), but the mechanisms are not clearly understood. Potassiumdichromate potentiated mutations produced by sodium azide in S. typhimurium or by 9-aminoacridine inS. typhimurium and E. coli. Although the data were insufficient for speculation on the specificbiochemical mechanism, it was suggested that the potentiation involved a specific effect of potassiumdichromate on the interaction of 9-aminoacridine or sodium azide with DNA or on subsequent DNAreplication and/or repair (LaVelle 1986a, 1986b). Nitrilotriacetic acid, which appears to have nogenotoxic potential itself, increased the frequencies of sister chromatid exchanges in Chinese hamsterovary cells and of micronuclei and chromosomal aberrations in cultured human lymphocytes that wereseen with lead chromate alone. However, nitrilotriacetic acid had no effect on the dose-related inductionof sister chromatid exchanges in Chinese hamster ovary cells that was seen with potassium chromatealone. It was suggested that nitrilotriacetic acid increased the solubility of the originally insoluble leadchromate, leading to increased uptake of the metal cation by the cells and subsequent increasedgenotoxicity (Montaldi et al. 1987). Nitrilotriacetic acid increased the frequency of point mutations inS. cerevisiae observed with a low concentration of sodium chromate, but decreased the frequency with afive-fold higher concentration of sodium chromate. It was suggested that at the low concentration ofsodium chromate, nitrilotriacetic acid affected the uptake of chromium(VI), favoring reduction tochromium(III) ions, which formed a complex with nitrilotriacetic acid that can cross the membrane andinteract with DNA. At the high dose of sodium chromate, nitrilotriacetic acid may have affected themechanism of recombination repair of DNA breaks induced by chromate oxidizing activity (Bronzetti andGalli 1989). Nitrilotriacetic acid also increased the mutagenicity of potassium dichromate inS. typhimurium and D. melanogaster presumably by favoring the reduction of chromium(VI) tochromium(III) (Gava et al.1989a). Thus, it is possible that other hazardous substances at hazardous wastesites may be more dangerous due to the presence of chromium(VI).Ascorbic acid has been shown to have a protective effect in rats administered lethal dermal doses ofpotassium dichromate (25 mg chromium(VI)/rat), and in preventing ulcerations of the skin (Samitz 1970).The nephrotoxicity due to subcutaneous injections of potassium chromate in rats was prevented byintramuscular administration of ascorbic acid (Powers et al. 1986). This occurred mainly through thereduction of chromium(VI) to the less toxic chromium(III) state. Vitamin E protected against, whilevitamin B 2 enhanced, the cytotoxicity and DNA strand breaks induced by sodium chromate in Chinesehamster cells in vitro. Vitamin E may exert its protective effect by scavenging radicals and/orchromium(V) during the reduction of chromium(VI) (Sugiyama 1991) (see Section 2.11.3).N-Acetylcysteine, the glutathione precursor, was reported to be effective in increasing the urinaryexcretion of chromium in rats (Nadig 1994).