Difference between kidney and liver in decreased manganese superoxide dismutase activity caused by exposure of mice to mercuric chloride

Shimojo, Naoki; Kumagai, Yoshito; Nagafune, Jun

doi:10.1007/s00204-002-0364-4

Cited by 17 publications

(13 citation statements)

References 24 publications

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“…Because approximately three fourths of the SOD activity in the mouse kidney is Cu,Zn SOD (29), this isoform accounts for at least part of the inhibition by HgCl 2 . Mn SOD activity is also inhibited in mice that receive an injection of HgCl 2 , which may act directly on the enzyme (30). Although HgCl 2 decreases SOD activity after 24 h, by 48 h the SOD activity returns to normal levels.…”

Section: Mechanism Of Action Of Dmsomentioning

confidence: 99%

Delayed DMSO Administration Protects the Kidney from Mercuric Chloride-Induced Injury

Jo¹,

Hu²,

Yuen³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Reactive oxygen species are implicated as mediators of tissue damage in ischemic and toxic acute renal failure. Whereas many agents can inhibit renal ischemic injury, only hepatocyte growth factor, melatonin, N-acetylcysteine, and DMSO inhibit injury after mercuric chloride administration. Although it has been suggested that DMSO may chelate the mercuric ion, more recent studies suggest that it has antiinflammatory and antioxidant effects. Acute renal failure was induced by 5 mg/kg subcutaneous injection of mercuric chloride in BALB/c mice. DMSO (3.8 ml/kg, 40% in PBS) or vehicle (PBS) was injected intraperitoneally at 0 and 24 h after mercuric chloride injection, or DMSO treatment was delayed 3 or 5 h. DMSO prevented increases in serum creatinine and tubular damage at 24 and 48 h. When DMSO treatment was delayed by 3 h, it was still beneficial; however, with a 5-h delay, the histology score and serum creatinine were not significantly decreased. DMSO partially prevented a mercuric chloride-induced decrease in glutathione peroxidase activity and completely prevented the transient decrease in superoxide dismutase activity. Neither mercuric chloride nor DMSO affected catalase activity significantly. For investigating possible effects of DMSO on cellular mercuric ion uptake, MDCK cells that were transfected with human organic anion transporter-1 were used. 203 Hg uptake was inhibited 90% by N-acetylcysteine but only 5% by DMSO, indicating that the effect of DMSO is not related to chelating mercuric ion or inhibiting its uptake. It is concluded that DMSO acts in part as an antioxidant to inhibit mercuric chloride-induced acute renal injury.

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Section: Mechanism Of Action Of Dmsomentioning

confidence: 99%

Delayed DMSO Administration Protects the Kidney from Mercuric Chloride-Induced Injury

Jo¹,

Hu²,

Yuen³

et al. 2004

Journal of the American Society of Nephrology

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“…2 The dissociated mercury from HgCl 2 is readily assimilated in each rat tissue (as seen in Table 2), and especially accumulates in kidney, which is in accord with previous reports. 20,21 Contrary to the above, the mercury contents in other tissues, including brain, heart and serum, were not significantly different among the different cinnabar groups (P < 0.05). The mercury contents in the erythrocyte and plasma fractions were negligible for all cinnabar groups, but they were significantly higher in the HgCl 2 group and almost the same in the two blood phases (about 0.7 µg g −1 in both erythrocyte and plasma fractions).…”

Section: Heavy Metals Determined With Icp-msmentioning

confidence: 68%

“…Rats were maintained in air-conditioned metabolic boxes in standard conditions (18)(19)(20)(21)(22)(23)(24) • C) on a 12 h/12 h light/darkness cycle. They were randomly divided into six groups, with 10 rats in each group.…”

Section: Animal Treatmentmentioning

confidence: 99%

“…The results, shown in Table 3, indicate an essentially quantitative recovery, with values ranging from 89.5 to 112%. The high affinity between mercury and thiolate (-SH) is the main reason why mercury is a strong poison to human 20 Conversely, the high affinity of mercury with -SH is one of the most important means to detoxify mercury, because the binding of Hg-SH in MT is one of the most important routes for mercury excretion. 23,24 The MT contents in each organ of the different rat groups shown in Table 3 indicate that large amounts of MT were induced in the liver and kidney of the cinnabar group IV and HgCl 2 group, in which the high contents of mercury in the two organs were observed in Table 2.…”

Section: Mt Concentrations In Rat Tissuesmentioning

confidence: 99%

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

Huang

Shen

Zhuang

et al. 2004

Applied Organom Chemis

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Cinnabar, 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 < 0.01). A high positive correlation observed between MT concentrations and mercury levels in both liver and kidney (R 2 = 0.9299, P < 0.02 for liver; R 2 = 0.9923, P < 0.0008 for kidney) indicated that MT could be used as a biomarker for mercury in tissues.

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“…Mercury is excreted almost exclusively via the kidney; thus, renal exposure to mercury is unavoidable and subsequent toxicity commonly evolves in the kidney (Madden & Fowler 2000). Renal mercury chloride (HgCl 2 )-induced damage has been studied using experimental models of nephropathy, showing that the toxic effects of HgCl 2 in the kidney are related to inflammatory events and/or oxidative stress (Ghielli et al 2000;Aleo et al 2002;Shimojo et al 2002;de Greef et al 2003;Stacchiotti et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Renal oxidative stress and renal CD8⁺ T-cell infiltration in mercuric chloride-induced nephropathy in rats: role of angiotensin II

Peña

Hernández-Fonseca

Pedreáñez

et al. 2015

Journal of Immunotoxicology

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Mercuric chloride (HgCl 2 ) induces kidney damage, in part, through oxidative stress. A role for angiotensin II (Ang II) in pro-inflammatory events in a model of acute HgCl 2 -induced nephropathy was reported. Ang II is a potent oxidative stress inducer; however, its role in oxidative/anti-oxidative events in HgCl 2 -induced nephropathy remains unknown. The aim of this study was to determine the role of Ang II in the oxidative stress and renal infiltration of CD8 + T-cells after an acute HgCl 2 intoxication. Three groups of Sprague Dawley rats were treated with a single subcutaneous dose of 2.5 mg/kg HgCl 2 : for 3 days prior to and for 4 days after that injection, rats in one group received Losartan (30 mg/kg), in another group Enalapril (30 mg/kg) or normal saline in the last group. Two other groups of drug-treated rats received saline in place of HgCl 2 . A final group of rats received saline in place of HgCl 2 and the test drugs. All treatments were via gastric gavage. At 96 h after the vehicle/HgCl 2 injection, blood and kidney samples were harvested. Renal sections were homogenized for measures of malondialdehyde (MDA), reduced glutathione (GSH) and catalase activity. Frozen sections were studied for the presence of superoxide anion (O À 2 ) and CD8 + T-cells. HgCl 2 -treated rats had increased interstitial and tubular expression of O À 2 , high levels of MDA, normal catalase activity and GSH content, increased levels of interstitial CD8 + T-cells and an increased percentage of necrotic tubules. Anti-Ang II treatments diminished the HgCl 2 -induced increases in interstitial O À 2 , CD8 + T-cells and tubular damage and increased catalase and GSH expression above that due to HgCl 2 alone; the HgCl 2 -induced high MDA levels were unaffected by the drugs. These data provide new information regarding the potential role of Ang II in the oxidative stress and renal CD8 + T-cell infiltration that occur during HgCl 2 nephropathy.ARTICLE HISTORY

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Difference between kidney and liver in decreased manganese superoxide dismutase activity caused by exposure of mice to mercuric chloride

Cited by 17 publications

References 24 publications

Delayed DMSO Administration Protects the Kidney from Mercuric Chloride-Induced Injury

Delayed DMSO Administration Protects the Kidney from Mercuric Chloride-Induced Injury

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

Renal oxidative stress and renal CD8⁺ T-cell infiltration in mercuric chloride-induced nephropathy in rats: role of angiotensin II

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Difference between kidney and liver in decreased manganese superoxide dismutase activity caused by exposure of mice to mercuric chloride

Cited by 17 publications

References 24 publications

Delayed DMSO Administration Protects the Kidney from Mercuric Chloride-Induced Injury

Delayed DMSO Administration Protects the Kidney from Mercuric Chloride-Induced Injury

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

Renal oxidative stress and renal CD8+ T-cell infiltration in mercuric chloride-induced nephropathy in rats: role of angiotensin II

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Resources

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Renal oxidative stress and renal CD8⁺ T-cell infiltration in mercuric chloride-induced nephropathy in rats: role of angiotensin II