Lipid Peroxidation and Antioxidant Enzyme Activity in Different Organs of Mice Exposed to Low Level of Mercury

Mahboob, M.; Shireen, Kaniz F.; Atkinson, Alfonza; Khan, Abu T.

doi:10.1081/pfc-100106195

Cited by 127 publications

(83 citation statements)

References 24 publications

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“…Binding to key enzymes and structural or functional proteins has been proposed to cause the Hg toxicity (Boadi et al, 1991). The effects of Hg on intracellular thiol metabolism, oxidative stress, lipid peroxidation, mitochondrial function, and intracellular distribution of calcium ions may also play a role in nephropathy induced by Hg (Mahboob et al, 2001;Zalups, 2000). In the current study, a dose of 0.25 mg/ kg Hg induced renal injury involving 25-50% of the proximal tubules while a dose of 0.5 mg/ kg Hg induced histopathologic lesions involving 50-75% of tubules.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Kidney Injury Molecule-1 and Other Nephrotoxicity Biomarkers in Urine and Kidney Following Acute Exposure to Gentamicin, Mercury, and Chromium

Zhou

Vaidya

Brown

et al. 2007

Toxicological Sciences

259

159

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Sensitive biomarkers are needed to detect kidney injury at the earliest stages. The objective of this study was to determine whether the appearance of kidney injury molecule-1 (Kim-1) protein ectodomain in urine and kidney injury molecule-1/hepatitis A viral cellular receptor-1 (Kim-1/ Havcr1) gene expression in kidney tissue may be more predictive of renal injury after exposure to nephrotoxicants when compared to traditionally used biomarkers. Male Sprague-Dawley rats were injected with a range of doses of gentamicin, mercury (Hg; HgCl 2 ), or chromium (Cr; K 2 Cr 2 O 7 ). The results showed that increases in urinary Kim-1 and kidney Kim-1/Havcr1 gene expression paralleled the degree of severity of renal histopathology and were detected at lower doses of nephrotoxicants when compared to blood urea nitrogen (BUN), serum creatinine, and urinary Nacetyl-β-D-glucosaminidase (NAG). In a time course study, urinary Kim-1 was elevated within 24 h after exposure to gentamicin (100 mg/kg), Hg (0.25 mg/kg), or Cr (5 mg/kg) and remained elevated through 72 h. NAG responses were nephrotoxicant dependent with elevations occurring early (gentamicin), late (Cr), or no change (Hg). At 72 h, after treatment with any of the three nephrotoxicants, there was increased Kim-1 immunoreactivity and necrosis involving ∼50% of the proximal tubules; however, only urinary Kim-1 was significantly increased, while BUN, serum creatinine, and NAG were not different from controls. In rats treated with the hepatotoxicant galactosamine (1.1 mg/kg), serum alanine aminotransferase was increased, but no increase in urinary Kim-1 was observed. Urinary Kim-1 and kidney Kim-1/Havcr1 expression appear to be sensitive and tissue-specific biomarkers that will improve detection of early acute kidney injury following exposure to nephrotoxic chemicals and drugs. Keywordsacute kidney injury; nephrotoxicity biomarkers; kidney injury molecule-1; mercury; chromium; gentamicin 1To whom correspondence should be addressed at Center for Devices and Radiological Health, U.S. Food and Drug Administration, White Oak Life Sciences Laboratory, WO64-4064, 10903 New Hampshire Avenue, Silver Spring, MD 20993-0002. Fax: 301-796-9826. E-mail: peter.goering@fda.hhs.gov.. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptRenal insufficiency, in some form, has been reported to occur in ∼11% of the U.S. population (Nally, 2002). Acute kidney injury (AKI) or acute renal failure (ARF) occurs in 2-5% of patients admitted to general hospitals in the United States, and AKI is associated with a high rate (up to 50%) of mortality (Chertow et al., 2005;Nally, 2002). The annual health care expenditures attributable to hospital-acquired AKI based on conservative assumptions are estimated to exceed $10 billion (Chertow et al., 2005). Patients with subclinical renal injury may be more sensitive to AKI following exposure to potentially nephrotoxic drugs and/or compounds released unintentionally from medical device materials (e.g., residues, le...

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Section: Discussionmentioning

confidence: 99%

Comparison of Kidney Injury Molecule-1 and Other Nephrotoxicity Biomarkers in Urine and Kidney Following Acute Exposure to Gentamicin, Mercury, and Chromium

Zhou

Vaidya

Brown

et al. 2007

Toxicological Sciences

259

159

View full text Add to dashboard Cite

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“…It is known that mercury (II) is a highly toxic metal which induces oxidative stress in the body [27,28]. Lipid peroxidation [8,29], attenuation of antioxidant defense depleting GSH and inhibiting the activities of antioxidant enzymes occur in the liver, kidney and other tissues of mice under HgCl 2 [5]. ROS are mediators of tissue damages in several animal species due to HgCl 2 .…”

Section: Modeling Of Mercury Accumulation In Liver Tissuesmentioning

confidence: 99%

Effects of Eriobotrya japonica (Lindl.) flower extracts on mercuric chloride-induced hepatotoxicity in rats

et al. 2012

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Mercury (II) is an important factor in hepatotoxicity that can enter the body through marine diets and amalgams. In the present study, the protective effect of the Eriobotrya japonica flower extract (EJFE) on HgCl 2 -induced hepatotoxicity was investigated. Five mg/kg of mercuric chloride in drinking water was given to rats either with saline or EJFE (100 and 200 mg/kg as intraperitoneal (IP)) for 30 d. The mercury levels in different groups of liver tissues of the rats were measured with flameless atomic absorption spectroscopy (F-AAS). Also, mercury accumulation in the liver of the rats was modeled by using a parallel chemical kinetic model. The results showed that HgCl 2 -induced oxidative damage led to a significant decrease in glutathione (GSH) and the total antioxidant capacity (TAC) levels, and to a significant increase in lipid peroxidation level. Accumulated mercury was 14.47% more in the livers of the stress groups than in those of the control groups (P<0.001), whereas the amount of Hg was adjusted to 13.49% and 13.93% in groups treated with 100 and 200 mg/kg of EJFE respectively, as compared with stress groups (P<0.001). HPLC analysis of EJFE revealed that hesperetin and gallic acid are the major antioxidants in EJFE. Results demonstrate that flowers of the Eriobotrya japonica cause a significant protection against HgCl 2 induced hepatotoxicity in all diagnostic parameters by strengthening the antioxidant defense mechanisms and they may have a therapeutic function in free radical mediated diseases. mercury, oxidative stress, hepatotoxic, Eriobotrya japonica, antioxidant Citation:Esmaeili A H, Khavari-Nejad R A, Hajizadeh Moghaddam A, et al. Effects of Eriobotrya japonica (Lindl.) flower extracts on mercuric chloride-induced hepatotoxicity in rats.

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“…In fact, HgCl 2 enhances the formation of reactive oxygen species (ROS, including hydrogen peroxides, lipid peroxides, and highly reactive hydroxyl radicals) (5), which may cause cell membrane damage and cell destruction (6). HgCl 2 depletes protective antioxidants (eg, glutathione) and inhibits the activities of free radical scavenging systems, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

The Hepatoprotective Effect of Gallic Acid on Mercuric Chloride-Induced Liver Damage in Rats

Goudarzi

Kalantar

2017

Jundishapur J Nat Pharm Prod

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Background: Mercury has a variety of industrial applications and is well-known for its hematotoxic, hepatotoxic, neurotoxic, nephrotoxic, and genotoxic effects. Objectives: This study was carried out to assess the protective effects of gallic acid against mercuric chloride-induced oxidative stress in albino rats. Methods: A total of 35 male Wistar rats were divided into 5 groups (7 rats per group). Groups 1 and 2 were used as the negative and positive controls, respectively and received normal saline (2 mL/kg/day, po) and mercuric chloride (0.4 mg/kg/day, po) for 28 days. Group 3 only received gallic acid (200 mg/kg/day, po) for 28 days, whereas groups 4 and 5 received gallic acid (50 and 200 mg/kg/day, respectively) after 1 hour, followed by mercuric chloride (0.4 mg/kg/day, po) for 28 days. Results:The results demonstrated that treatment with gallic acid significantly diminished the mercuric chloride-induced increase in the serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and lipid peroxidation in liver tissues. In addition, gallic acid treatment increased the level of glutathione peroxidase, superoxide dismutase, and catalase activity and lowered the glutathione level in liver tissues, compared to the mercuric chloride group. The liver of rats, treated with mercuric chloride, showed degenerated cells (with mild cytoplasmic vacuolation and blebbing), binucleated cells, and significant sinusoidal dilation. Conclusions: It can be concluded that gallic acid restores the activities of antioxidant enzymes and tissue markers in mercuric chloride-treated rats, probably by scavenging free radicals and improving the antioxidant defense mechanisms.

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Lipid Peroxidation and Antioxidant Enzyme Activity in Different Organs of Mice Exposed to Low Level of Mercury

Cited by 127 publications

References 24 publications

Comparison of Kidney Injury Molecule-1 and Other Nephrotoxicity Biomarkers in Urine and Kidney Following Acute Exposure to Gentamicin, Mercury, and Chromium

Comparison of Kidney Injury Molecule-1 and Other Nephrotoxicity Biomarkers in Urine and Kidney Following Acute Exposure to Gentamicin, Mercury, and Chromium

Effects of Eriobotrya japonica (Lindl.) flower extracts on mercuric chloride-induced hepatotoxicity in rats

The Hepatoprotective Effect of Gallic Acid on Mercuric Chloride-Induced Liver Damage in Rats

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