Acute Depletion and Recovery of Peritoneal B-1 Lymphocytes in BALB/c Mice after a Single Injection of Mercury Chloride

Madureira, Pedro; Cunha, Elisabete M; Águas, Artur P.

doi:10.1080/08923970701513518

Cited by 7 publications

(5 citation statements)

References 33 publications

(38 reference statements)

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“…The rise in creatinine level might be This elevation in above said parameters has been well due to damage produce in kidney tubules by mercury. Madureira et al, [19], Hounkpatin et al, [20]. The groups on 28th day post-treatment as compare to decreased in Hb, PCV and TEC might due to the control of that group.…”

Section: Discussionmentioning

confidence: 99%

Repeated dose oral toxicity of inorganic mercury in wistar rats: biochemical and morphological alterations

Sheikh¹,

Patel²,

Joshi³

et al. 2013

Vet World

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Aim: The study was conducted to find out the possible toxic effect of mercuric chloride (HgCl2 ) at the histological, biochemical, and haematological levels in the wistar rats for 28 days. Materials and Methods: The biochemical and hematological alteration were estimated in four groups of rat (each group contain ten animals), which were treated with 0 (control), 2, 4, and 8 mg/kg body weight of HgCl2 through oral gavage. At the end of study all rats were sacrificed and subjected for histopathology. Result: A significantly (P < 0.05) higher level of serum alanine amino transferase (ALT), gamma Glutamyle Transferase, and creatinine were recorded in treatment groups, while the level of alkaline phosphtase (ALP) was significantly decreased as compared to the control group. The toxic effect on hematoclogical parameter was characterized by significant decrease in hemoglobin, packed cell volume, total erythrocytes count, and total leukocyte count. Gross morphological changes include congestion, severe haemorrhage, necrosis, degenerative changes in kidneys, depletion of lymphocyte in spleen, decrease in concentration of mature spermatocyte, and edema in testis. It was notable that kidney was the most affected organ. Conclusion: Mercuric chloride (HgCl ) caused dose-dependent toxic effects on blood parameters and kidney. [Vet World 2013; 6(8.000): 563-567

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Section: Discussionmentioning

confidence: 99%

Repeated dose oral toxicity of inorganic mercury in wistar rats: biochemical and morphological alterations

Sheikh¹,

Patel²,

Joshi³

et al. 2013

Vet World

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show abstract

“…2017; 12(4):e12345. 5 level of GSH, which is the primary line of cellular protection against toxic agents and major intracellular conjugation factors, reduced and displayed damaged function in Hg toxicity (31,32). Binding of HgCl 2 to GSH reduces GSH level in the cells and decreases the antioxidant capacity of the cells (33).…”

Section: Discussionmentioning

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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“…Our finding of the synergistic effect between Pb and inflammation in liver agrees entirely with the previous investigations, which studied the effect between other toxic agents such as heavy metals and inflammation. For instance, the synergistic response between monocrotaline and LPS (Yee et al, 2000), between S-adenosyl- l -methionine and CYP2EI (Wang and Cederbaum, 2005), between trovafloxacin and LPS (Waring et al, 2006), between Aroclor and LPS (Brown et al, 1996), between cocaine and LPS (Labib et al, 2002), between B-1 lymphocytes and Hg (Madureira et al, 2007) and between Hg and LPS (Rumbeiha et al, 2000). We can conclude that the effect between Pb and inflammation in this study is a synergistic response.…”

Section: Discussionmentioning

confidence: 99%

Lead hepatotoxicology

Sa¹,

Costa

Cunha³

2011

Toxicol Ind Health

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The increasing use of lead (Pb) for industrial purposes has resulted in the significant increase in environmental contamination of our planet especially in concern to water and food. In this study using the electron scanning microscopy (SEM), the authors showed the effects of this metal as a result of a chronic and cumulative process. As a primary method of detection of Pb in situ, SEM was chosen, coupled with a detection system Noran Voyager of basic microanalysis X-ray (SEM-XRM), with detection system energy dispersive spectrometry. Mice BALB/c was used as a study model. An animal model of inflammation was used, that consisted in the formation of a subcutaneous pocket of air. It was observed that 75% of Pb stock was captured by the liver, the main target organ in the capture of the metal, the kidney was the second organ to capture the Pb stock and the third was the spleen. It was verified that a low deposition of Pb was found in the lungs and the brain. The main results of this study showed how Pb is captured by different organs. We also demonstrated the vulnerability to inflammation of this metal.

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Acute Depletion and Recovery of Peritoneal B-1 Lymphocytes in BALB/c Mice after a Single Injection of Mercury Chloride

Cited by 7 publications

References 33 publications

Repeated dose oral toxicity of inorganic mercury in wistar rats: biochemical and morphological alterations

Repeated dose oral toxicity of inorganic mercury in wistar rats: biochemical and morphological alterations

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

Lead hepatotoxicology

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