Mercury chloride increases hepatic alanine aminotransferase and glucose 6‐phosphatase activities in newborn rats<i>in vivo</i>

Moraes-Silva, Lucélia; Bueno, Tania Maria; Franciscato, Carina; Oliveira, Cláudia S.; Peixoto, Nilce Coelho; Pereira, Maria Estér

doi:10.1042/cbi20100475

Cited by 13 publications

(12 citation statements)

References 32 publications

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“…Although mercury has long been considered a toxic metal, it still has numerous important industrial uses and poisoning from occupational exposure and environmental pollution continues to be a concern [2]. In several in vitro and in vivo studies, damaging effects induced by mercury were related to adverse health impacts including cancer, neurological disorders and cardiovascular diseases [3–4]. Among organs, the liver is the major site for handling toxins, with a central role in physiological metabolism and various detoxification reactions.…”

Section: Introductionmentioning

confidence: 99%

Dietary luteolin attenuates chronic liver injury induced by mercuric chloride via the Nrf2/NF-κB/P53 signaling pathway in rats

et al. 2017

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Mercury exposure is a common cause of metal poisoning which is biotransformed to highly toxic metabolites thus eliciting biochemical alterations and oxidative stress. Luteolin, a phenolic compound found in many natural products, has multiple biological functions. Our study was aimed to explore the biological effects of luteolin in a liver injury model induced in rats by mercuric chloride (HgCl2). Criteria for injury included liver enzyme, glutathione and malondialdehyde levels, histopathology, TUNEL assay, hepatocyte viability and reactive oxygen species levels. The results showed that luteolin protected against HgCl2-induced liver injury. Luteolin increased total nuclear factor-erythroid-2-related factor 2 (Nrf2) levels in the presence of HgCl2. Upregulation of its downstream factors, heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1, was also observed. This suggested that protection by luteolin against HgCl2-induced liver injury involved Nrf2 pathway activation. Luteolin also decreased expression of nuclear factor-κB (NF-κB) and P53. HgCl2 exposure led to increased Bcl-associated X protein (Bax), and decreased Bcl-2-related protein long form of Bcl-x (Bcl-xL) and B-cell leukemia/lymphoma-2 (Bcl-2) expression, leading to an increased Bax/Bcl-2 ratio. Taken together, our data suggested that decreasing oxidative stress is a protective mechanism of luteolin against development of HgCl2-induced liver injury, through the Nrf2/NF-κB/P53 signaling pathway in rats.

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Section: Introductionmentioning

confidence: 99%

Dietary luteolin attenuates chronic liver injury induced by mercuric chloride via the Nrf2/NF-κB/P53 signaling pathway in rats

et al. 2017

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“…LDH is a cytosolic enzyme that catalyses the reversible oxidation of l ‐lactate to pyruvate; its increased activity in serum confirms increased hepatocyte membrane permeability and cellular damage . ALT and aspatate aminotransferase are two reliable markers for hepatic toxicity and showed peak values after MeHg administration . In this study, the ZPDC glycoprotein inhibits elevated serum enzymes (LDH and ALT) in mercury‐chloride‐induced primary cultured hepatocytes.…”

Section: Discussionmentioning

confidence: 72%

“…24 ALT and aspatate aminotransferase are two reliable markers for hepatic toxicity and showed peak values after MeHg administration. 25 In this study, the ZPDC glycoprotein inhibits elevated serum enzymes (LDH and ALT) in mercury-chloride-induced primary cultured hepatocytes.…”

Section: Discussionmentioning

confidence: 80%

Preventive effects of ZPDC glycoprotein (24 kDa) on hepatotoxicity induced by mercury chloride in vitro and in vivo

Liu

Lee

Lim

2014

Cell Biochemistry & Function

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Mercury is a potent environmental contaminant that exerts toxic effect on various vital organs in the human body. Recently, we isolated glycoprotein from Zanthoxylum piperitum DC (ZPDC), which has antioxidant and anticancer effects. In the present study, we determined the preventive effects of ZPDC glycoprotein on hepatic damage induced by mercury chloride (HgCl2 ). We evaluated the activities of lactate dehydrogenase (LDH), alanine aminotransferase (ALT), antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)], extracellular signal-regulated kinase (ERK)1/2, p38 mitogen-activated protein kinase (MAPK), cyclo-oxygenase (COX-2), inducible nitric oxide synthetase (iNOS), and activator protein (AP-1) and the quantitative expressions of nuclear factor E2-related factor (Nrf2), heme oxygenase (HO-1), metallothionein (MT) and reduced glutathione (GSH) in mercury-chloride-exposed (50 μM and 10 mg/kg body weight) primary cultured hepatocytes and ICR mice, using biochemical assays, radioactivity and immunoblot analysis. The results demonstrated that ZPDC glycoprotein decreased the levels of LDH, ALT, HO-1 and MT, whereas it increased the activities of hepatic antioxidant enzymes (SOD, CAT and GPx) and reduced GSH in mercury-chloride-exposed primary cultured hepatocytes. Also, it suppressed arachidonic acid release and expression of ERK, p38 MAPK, COX-2, iNOS, AP-1 and Nrf-2 in primary cultured hepatocytes and ICR mice exposed to mercury chloride. Collectively, ZPDC glycoprotein may have potential applications to prevent hepatotoxicity induced by mercury chloride.

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“…The previous exposure to copper only prevented the increase of serum creatinine but not the other metabolic parameters. In fact, the Hg-intoxicated rats presented lower growth than other groups, which can reflect the increase in the protein catabolism in an attempt to maintain the gluconeogenesis route [37]. Moreover, zinc also prevented the increase of urea level induced by Hg [4,5].…”

Section: Discussionmentioning

confidence: 95%

Effectiveness of copper chloride in protecting against alterations induced by mercury chloride in newborn rats

Moraes-Silva

Bueno

Franciscato

et al. 2012

J Biochem & Molecular Tox

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This work investigated the effects of copper as preventive treatment against mercury-induced alterations in young rats. Wistar rats were treated (subcutaneous) with saline or CuCl(2) · 2H(2) O (6.9 mg/kg/day) from 3 to 7 days old and with saline or HgCl(2) (5.0 mg/kg/day) from 8 to 12 days old. Rats were sacrificed 24 h after the last dose. Mercury-exposed rats presented inhibition of liver (43%) and kidney (52%) porphobilinogen (PBG)-synthase activity and serum lactic dehydrogenase activity (50%). Also, an increase of the serum creatinine and urea levels around threefold and fivefold was observed, respectively. Pre-exposure to copper partially prevented the mercury effect on liver but not on kidney PBG synthase, and prevented the increase of the creatinine levels. Blood and brain PBG synthase and serum alanineaminotransferase activities, as well as glycemia, and liver glycogen content were not altered by treatments. These results show that copper, although being an essential metal, is inefficient as a preventive agent against mercury poisoning in parameters investigated after the end of mercury exposure.

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Mercury chloride increases hepatic alanine aminotransferase and glucose 6‐phosphatase activities in newborn ratsin vivo

Cited by 13 publications

References 32 publications

Dietary luteolin attenuates chronic liver injury induced by mercuric chloride via the Nrf2/NF-κB/P53 signaling pathway in rats

Dietary luteolin attenuates chronic liver injury induced by mercuric chloride via the Nrf2/NF-κB/P53 signaling pathway in rats

Preventive effects of ZPDC glycoprotein (24 kDa) on hepatotoxicity induced by mercury chloride in vitro and in vivo

Effectiveness of copper chloride in protecting against alterations induced by mercury chloride in newborn rats

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