Mercury Concentrations In Kidney Research Articles

Mercury concentrations in Common Tern Sterna hirundo and Slender-billed Gull Larus genei from the Shadegan Marshes of Iran, in north-western corner of the Persian Gulf.

We examined mercury levels in several tissues of Common Terns and Slender-billed Gulls collected from Shadegan Marshes of south-western Iran. In both species, total mercury content was highest in feathers followed by liver, kidney and muscle tissue. We found a significant correlation between mercury concentrations in kidney and breast feather (r=0.83, p<0.05), breast feather and liver (r=0.81, p<0.05) as well as liver and kidney (r=0.83, p<0.05). The contaminant levels in the feathers (11.53 and 15.32 μg/g in breast feather and tail feather, respectively) of Common Terns from Shadegan Marshes are higher than those reported for other tern species from elsewhere in the world, but feather mercury of Slender-billed Gull (6.61 and 5.35 μg/g in breast feather and tail feather, respectively) was similar to those reported for gull species worldwide. Mean values for mercury in the feather of two seabird species were higher than the levels known to cause adverse effects.

Diversity of total mercury concentrations in kidneys of birds from Eastern Poland.

Diversity of total mercury concentrations in kidneys of birds from Eastern Poland.

Metallothionein as a biomarker for mercury in tissues of rat fed orally with cinnabar

AbstractCinnabar, as one of the most widely used mineral drugs in traditional Chinese medicines, has been proven to have prominent curative effects in clinical use for more than 2000 years. But the safety and toxicity of the drug has been under constant debate in clinic usage. Metallothionein (MT) contains about 30% of cysteine in the molecule, and plays an important detoxification role against heavy metals. In this study, it was used as a biomarker to assess mercurial accumulation in rats fed orally with cinnabar. After feeding rats with cinnabar by gastric gavage at different dosages and at different times, the distribution of heavy metals (including mercury, copper and zinc) and MT was investigated among rat tissues, including liver, kidney, heart, brain, testis and blood. Metals and MT determinations were carried out using inductively coupled plasma mass spectrometry (ICP‐MS) and a modified mercury saturation assay technique respectively. The results indicated that mercury was easily accumulated in the tissues of rats exposed to cinnabar, especially in kidney. For example: at a feeding dosage of 5 g kg−1 (bw) for 4 weeks, the mercury concentrations in kidney were 13, 8.7, 21.6 and 26 times those in liver, testis, brain and heart respectively; and at 2.5 g kg−1 (bw) for 2 weeks, the mercury concentrations in kidney were 21, 2.1, 3 and 21 times those in liver, testis, brain and heart respectively. In addition, mercury in kidney and liver of all cinnabar groups was significantly higher than that of the control group (P &lt; 0.01). A high positive correlation observed between MT concentrations and mercury levels in both liver and kidney (R2 = 0.9299, P &lt; 0.02 for liver; R2 = 0.9923, P &lt; 0.0008 for kidney) indicated that MT could be used as a biomarker for mercury in tissues. Copyright © 2004 John Wiley &amp; Sons, Ltd.

Effects of 2,3-dimercapto-1-propanesulfonic acid (DMPS) on tissue and urine mercury levels following prolonged methylmercury exposure in rats.

Methylmercury, a potent neurotoxicant, accumulates in the brain as well as the kidney during chronic exposure. We evaluated the capacity of 2,3-dimercapto-1-propanesulfonic acid (DMPS), a tissue-permeable metal chelator, to reduce brain, kidney, and blood Hg levels and to promote Hg elimination in urine following exposure of F-344 rats to methylmercury hydroxide (MMH) (10 ppm) in drinking water for up to 9 weeks. Inorganic (Hg2+) and organic (CH3Hg+) mercury species in urine and tissues were assayed by cold vapor atomic fluorescence spectroscopy (CVAFS). Following MMH treatment for 9 weeks, Hg2+ and CH3Hg+ concentrations were 0.28 and 4.80 microg/g in the brain and 51.5 and 42.2 microg/g in the kidney, respectively. Twenty-four hours after ip administration of a single DMPS injection (100 mg/kg), kidney Hg2+ and CH3Hg+ declined 38% and 59%, whereas brain mercury levels were slightly increased, attributable entirely to the CH3Hg+ fraction. Concomitantly, Hg2+ and CH3Hg+ in urine increased by 7.2- and 28.3-fold, respectively, compared with prechelation values. A higher dose of DMPS (200 mg/kg) was no more effective than 100 mg/kg in promoting mercury excretion. In contrast, consecutive DMPS injections (100 mg/kg) given at 72-h intervals significantly decreased total mercury concentrations in kidney, brain, and blood. However, the decrease in brain and blood mercury content was restricted entirely to the CH3Hg+ fraction, consistent with the slow dealkylation rate of MMH in these tissues. Mass balance calculations showed that the total amount of mercury excreted in the urine following successive DMPS injections corresponds quantitatively to the total amount of mercury removed from the kidney, brain, and blood of MMH-exposed rats. These findings confirm the efficacy of consecutive DMPS treatments in decreasing mercury concentrations in target tissue and in reducing overall mercury body burden. They demonstrate further that the capacity of DMPS to deplete tissue Hg2+ is highly tissue-specific and reflects the relative capacity of the tissue for methylmercury dealkylation. In light of this observation, the inability of DMPS to reduce Hg2+ levels in brain or blood may explain the inefficacy of DMPS and similar chelating agents in the remediation of neurotoxicity associated with prolonged MMH exposure.

In vivo XRF analysis of mercury: the relation between concentrations in the kidney and the urine

The objective of this study was to determine the concentrations of mercury in organs of occupationally exposed workers using in vivo X-ray fluorescence analysis. Twenty mercury exposed workers and twelve occupationally unexposed referents participated in the study. Their mercury levels in kidney, liver and thyroid were measured using a technique based on excitation with partly plane polarized photons. The mercury levels in blood and urine were determined using atomic absorption spectrophotometry. The detection limit for mercury in the kidney was exceeded in nine of the exposed workers, but in none of the referents. The mean kidney mercury concentration (including estimates below the detection limits) was 24 mu g g-1 in the exposed workers, and 1 mu g g-1 in the referents. The association between mercury in the kidney and in urine was statistically significant, but it was unclear whether the relation was linear. The measurements on liver (n=10) and thyroid (n=8) in the exposed workers showed mercury levels below the detection limit. The study shows that it is now possible to measure the mercury concentrations in kidneys of occupationally exposed persons, using in vivo X-ray fluorescence. The estimated concentrations are in reasonable agreement with the limited human autopsy data, and the results of animal studies.

Thiol antidote to inorganic mercury toxicity with an uncharacteristic mechanism

α-Mercapto-β-(2-furyl)acrylic acid (MFA) significantly reduced the lethality of mercuric chloride to rats (2.2 mg Hg/kg, ip) when administered (25 mg/kg, po) at 1, 24, 48, and 72 hr. Daily administration of MFA (25 mg/kg, po) significantly reduced the lethality of daily injection of increasing amounts of mercuric chloride (1 mg Hg/kg × 7 days, 2 mg Hg/kg × 7 days, 4 mg Hg/kg × 14 days, ip). Mercury concentration in kidneys of MFA-treated rats was significantly higher than in vehicle-treated controls, whereas concentration in liver was (nonsignificantly) lower. Enhanced mercury deposition in kidney as a manifestation of antidotal effect is not characteristic of thiol chelators used in practice for mercury poisoning.

Effects of l- or d-cysteine coadministration on short-term distribution of inorganic mercury in the rat

Male Sprague-Dawley rats received iv injections of mercuric chloride alone or in combination with l-cysteine or d-cysteine. Mercury concentrations in kidney, liver, and cerebrum 5 min after injection increased linearly over the dose range of 0.1, 0.5, 1.0, and 2.0 μmol of mercury/kg. Over this dose range, coadministration of l-cysteine or d-cysteine at a 2-to-1 molar ratio relative to mercury increased renal mercury concentrations and reduced mercury accumulation in the liver, cerebrum, and erythrocytes. Renal mercury concentrations were highly correlated with plasma mercury concentrations 5 min after injection and coadministration of l-cysteine or d-cysteine did not alter this relationship. Hepatic and cerebral mercury concentrations were also highly correlated with plasma mercury concentrations but coadministration of either thiol compound altered the relationship between plasma and tissue mercury concentrations. These data suggested that different processes underlie short-term mercury accumulation in different tissues. Investigations of the effects on tissue distribution of various molar ratios of l- or d-cysteine relative to mercury further suggested that direct complexation of mercury by either thiol may be a critical factor in the control of mercury deposition in these tissues.

Mercury Metabolism in Japanese Quail I: The Effect of Dietary Mercury and Selenium On Their Tissue Distribution

Immature and adult coturnix quail were fed isolated soybean protein diets to which methylmercuric chloride or mercuric chloride were added with or without supplemental selenium for seven days. Samples of brain, blood, liver, and kidney were analyzed for total mercury and selenium via atomic absorption spectrophotometry. Selenium addition had no effect on the mercury concentration in kidney, brain, or blood but did tend to increase the concentration of mercury in the livers of the methylmercuric chloride-treated birds. Selenium in the presence of methylmercury increased the selenium concentration of liver and kidney but had little effect on the selenium concentration of brain or blood. Methylmercuric chloride supplementation resulted in increased selenium concentration in the blood of the selenium supplemented group. All other tissue selenium levels were unaffected by the addition of mercury.