Lipid peroxidation in rats administrated with mercuric chloride

Huang, Yeou‐Lih; Cheng, Su-Ya; Lin, Te-Hsien

doi:10.1007/bf02789461

Cited by 98 publications

(63 citation statements)

References 19 publications

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“…As a consequence, an imbalance in antioxidant protective mechanisms takes place, leading to oxidative stress in the cells. In fact, a drastic increase in reactive oxygen species production has been reported during acute treatment with HgCl 2 , inducing LPO in rat brain (7). In the present study, we also observed an increase in systemic LPO levels during the second week of treatment ( Figure 1A), possibly as a consequence of the depletion of antioxidants.…”

supporting

confidence: 82%

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

Gutiérrez-Carrasquilla

Mazzotti

Araújo

et al. 2006

Braz J Med Biol Res

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The present study was designed to evaluate the time course changes in peripheral markers of oxidative stress in a chronic HgCl 2 intoxication model. Twenty male adult Wistar rats were treated subcutaneously daily for 30 days and divided into two groups of 10 animals each: Hg, which received HgCl 2 (0.16 mg kg -1 day -1 ), and control, receiving the same volume of saline solution. Blood was collected at the first, second and fourth weeks of Hg administration to evaluate lipid peroxidation (LPO), total radical trapping antioxidant potential (TRAP), and superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase (CAT). HgCl 2 administration induced a rise (by 26%) in LPO compared to control (143 ± 10 cps/mg hemoglobin) in the second week and no difference was found at the end of the treatment. At that time, GST and GPx were higher (14 and 24%, respectively) in the Hg group, and Cu,Zn-SOD was lower (54%) compared to control. At the end of the treatment, Cu,Zn-SOD and CAT were higher (43 and 10%, respectively) in the Hg group compared to control (4.6 ± 0.3 U/mg protein; 37 ± 0.9 pmol/mg protein, respectively). TRAP was lower (69%) in the first week compared to control (43.8 ± 1.9 mM Trolox). These data provide evidence that HgCl 2 administration is accompanied by systemic oxidative damage in the initial phase of the process, which leads to adaptive changes in the antioxidant reserve, thus decreasing the oxidative injury at the end of 30 days of HgCl 2 administration. These results suggest that a preventive treatment with antioxidants would help to avoid oxidative damage in subjects with chronic intoxication.

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supporting

confidence: 82%

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

Gutiérrez-Carrasquilla

Mazzotti

Araújo

et al. 2006

Braz J Med Biol Res

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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%

“…It may end up decreased glutathione levels, an increase to ROS such as superoxide anion radical, hydrogen peroxide and hydroxyl radical [7], which induce lipid, protein, and DNA oxidation. Mercury exposure induces lipid peroxidation detected by increasing thiobarbituric acid reactive substances (TBARS) in tissues of kidneys, liver and brain in rats [8]. Moreover, HgCl 2 -induced injury can be ameliorated by enzymatic antioxidants such as superoxide dismutase, catalase and glutathione peroxidase [9] and non-enzymatic antioxidants such as plant antioxidants.…”

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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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“…Because of the high bonding affinity between mercury and sulfur, mercury binds to metallothioneins and small molecular weight thiols such as cysteine 5) and glutathione 6) . Mercury exposure has also been demonstrated to induce lipid peroxidation detected by increased thiobarbituric acid reactive substances (TBARS) in liver, kidney, brain and other tissues [7][8][9] . Mercury is known to increase the intracellular levels of reactive oxygen species such as superoxide 10) and hydrogen peroxides 11) , which induce oxidative stress, resulting in tissue damaging effects 12) .…”

Section: Introductionmentioning

confidence: 99%

Role of Selenium in Mercury Intoxication in Mice

Agarwal

Behari

2007

Ind Health

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Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 µ µ µ µ µmole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.

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Lipid peroxidation in rats administrated with mercuric chloride

Cited by 98 publications

References 19 publications

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

Peripheral markers of oxidative stress in chronic mercuric chloride intoxication

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

Role of Selenium in Mercury Intoxication in Mice

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