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TOXICOLOGICAL PROFILE FOR CHROMIUM - Davidborowski.com

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<strong>CHROMIUM</strong> 2292. HEALTH EFFECTSRecent studies have examined the effects of interactions between chromium and arsenic on bloodcholesterol and glucose levels and changes in organ weight in rats (Aguilar et al. 1997). Groups of fivemale Wistar rats were given food containing 5 µg/g of either arsenic(V) oxide, chromium(III) chloride, ora <strong>com</strong>bination of both chemicals for 10 weeks. Organ weight to body weight ratios of liver, spleen, lung,kidney, and heart were similar to control values for the three exposed groups. Arsenic alone increased thecholesterol blood level from 47.27(±6.85 SD) mg/dL in the control group to 96.83(±6.11). The<strong>com</strong>bination of arsenic and chromium reduced the blood cholesterol level to 46.69(±6.11 SD) mg/dL.Neither chemical alone or in <strong>com</strong>bination effected blood glucose levels. In most tissues the <strong>com</strong>binationof chemicals reduced the chromium level appreciably below control values. Supplemental chromiumincreased arsenic levels in liver, kidney, spleen, heart, and red blood cells, and reduced levels of arsenicin lung and hair tissues. Chromium did not appear to alter concentrations of arsenic in the liver.A study examining the chromium(VI) reduction in microsomes noted that the level of iron in the testsystem markedly influenced the V max of chromium(VI) reduction, suggesting that coexposure tochromium(VI) and agents that increase intracellular iron might lead to increased risk for chromium(VI)toxicity (Myers and Myers 1998).The effects of chromium(III) chloride and sodium chromate(VI) on the hepatotoxicity of carbontetrachloride exposure to mouse hepatocytes were examined by Tezuka et al. (1995). Primary cultures ofmouse hepatocytes were pretreated with 10 or 100 µM chromium for 24 hours followed by exposure to1–5 mM carbon tetrachloride for up to 1 hour. Chromium(VI) pretreatment significantly reduced the celltoxicity as well as lipid peroxidation caused by carbon tetrachloride. Chromium(III) pretreatment did nothave any effect on cell toxicity. About 50% of chromium(VI) was taken up and reduced in the cells by90% to chromium(III) within 10 minutes. The initial uptake rate of chromium(III) into cells was greaterthan 500-fold less than chromium(VI), and only about 5% was absorbed. The protection against carbontetrachloride damage by chromium(VI) was attributed to its rapid uptake and conversion tochromium(III), and it was determined that chromium(III) acts as a radical scavenger for the free radicalsgenerated by carbon tetrachloride within the cell. Furthermore, chromium(VI) pretreatment reduced theactivity of NADPH cytochrome c reductase which metabolizes carbon tetrachloride to reactive species.In a previous study (Tezuka et al. 1991), the same group found that pretreating mice and rats withchromium(III) also protected against hepatic toxicity.In order to examine the speciation of chromium in lemonade, Kool Aid, tea, dripped coffee, percolatedcoffee, and orange juice, potassium chromate(VI) was added to each of the beverages at a chromium

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