Comparative Effect of Silymarin and D-Penicillamine on Lead Induced Hemotoxicity and Oxidative Stress in Rat

Jalali, Seyedeh Missagh; Najafzadeh, Hossein; Mousavi, Seyedeh Maryam

doi:10.29252/arakmu.11.3.11

Cited by 8 publications

(6 citation statements)

References 30 publications

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“…Exposure of rats to lead Yusuf et al 11 induced a significant increase in erythrocyte osmotic fragility (EOF) in the experimental animals. This result is in line with previous studies as carried out by Jalali et al (2017), who found similar results as that reported in this study. The increase could be ascribed to the increase in the generation of reactive oxygen species (ROS) following oxidative damage, as caused by lead.…”

Section: Discussionsupporting

confidence: 83%

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Lead-induced increase in erythrocyte osmotic fragility and malondialdehyde concentration in Wistar rats: Chemo-protective effects of flavonoid mixture

Yusuf¹,

Akefe²,

Mohammed³

et al. 2018

Biochem Biotechnol Res

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Lead has been affirmed as a potent toxicant impairing physiological functions and causing innumerable perturbations at cellular and tissue levels. Daflon ® 500 mg is a flavonoid fraction of Rutaceae aurantiae comprising 90% diosmin and 10% hesperidin. The aim of this study was to evaluate the effect of flavonoid mixture against cellular injury caused by lead-induced generation of free radicals. Forty adult male Wistar rats divided into five groups of eight animals each were used for the experiment. Group I was administered distilled water only. Group II: lead (250 mg/kg BW), group III: lead (250 mg/kg BW) followed by dimercaptosuccinic acid (DMSA) (10 mg/kg BW), group IV: lead (250 mg/kg BW) followed by Daflon ® (100 mg/kg BW) and group V: lead (250 mg/kg BW) followed by Daflon ® (100 mg/kg BW) and DMSA (10 mg/kg BW). The xenobiotics were all administered orally. At the end of four weeks, EDTA-blood samples and serum samples were collected from the rats, and were used to evaluate changes in erythrocyte osmotic fragility and lipid peroxidation, respectively. Experimental exposure of rats to lead caused an increase in erythrocyte osmotic fragility (EOF) and lipid peroxidative changes, while administration of Daflon ® ameliorated the ensued damages. In conclusion, is plausible that the flavonoid mixture alleviated the detrimental effects of lead toxicity via its membrane stabilization, cytoprotective and osmoregulatory potentials.

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Section: Discussionsupporting

confidence: 83%

“…Tissue damage has also been reported in the pathophysiology of lead poisoning, with increasing evidence that oxidative stress plays an important role in the pathology of lead poisoning (Jalali et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Lead-induced increase in erythrocyte osmotic fragility and malondialdehyde concentration in Wistar rats: Chemo-protective effects of flavonoid mixture

Yusuf¹,

Akefe²,

Mohammed³

et al. 2018

Biochem Biotechnol Res

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“…Among the parts of the human body and systems hematopoietic, renal, reproductive, and central nervous systems are more vulnerable toward the dangers from exposure to high levels of lead. 4 According to Jalali et al (2017), the elevation of malondialdehyde (MDA) level increases erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities along with a rise in total leukocyte, lymphocyte, and neutrophil counts, resulting into microcytic anemia in the lead treated rats. 5 Chelation therapy is the conventional suggestion for low-level lead poisoning with brain (encephalopathic) damage.…”

Section: Introductionmentioning

confidence: 99%

“…4 According to Jalali et al (2017), the elevation of malondialdehyde (MDA) level increases erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities along with a rise in total leukocyte, lymphocyte, and neutrophil counts, resulting into microcytic anemia in the lead treated rats. 5 Chelation therapy is the conventional suggestion for low-level lead poisoning with brain (encephalopathic) damage. However, the treatment with low amounts but for longer duration is still under investigation.…”

Section: Introductionmentioning

confidence: 99%

Biochemical and Molecular Bases of Lead-Induced Toxicity in Mammalian Systems and Possible Mitigations

Singh

Kumar

Gupta

et al. 2018

Chem. Res. Toxicol.

115

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The effects of lead exposure on mammals are reported to be devastating. Lead is present in all the abiotic environmental components such as brass, dust, plumbing fixtures, soil, water, and lead mixed imported products. Its continuous use for several industrial and domestic purposes has caused a rise in its levels, thereby posing serious threats to human health. The mechanisms involved in lead-induced toxicity primarily include free-radical-mediated generation of oxidative stress which directly imbalances the prooxidants and the antioxidants in body. The toxicity of lead involves damage primarily to major biomolecules (lipid, protein, and nucleic acids) and liver (hepatotoxicity), nervous system (neurotoxicity), kidney (nephrotoxicity) and DNA (genotoxicity), present in animals and humans. The activation of c-Jun NH2-terminal kinase, phosphoinositide 3-kinase, or Akt and p38 mitogen activated protein kinase signaling pathways are important for lead cytotoxicity. Lead increased apoptosis through signaling cascade and associated factors and significantly impairs cell differentiation and maturation. In addition, lead has great impact on metabolic pathways such as heme synthesis, thereby leading to the onset of anemia in lead exposed people. This review encompasses an updated account of varied aspects of lead-induced oxidative stress and the biomolecular consequences such as perturbations in physiological processes, apoptosis, carcinogenesis, hormonal imbalance, loss of vision, and reduced fertility and their possible remediation through synthetic (chelators) and natural compounds (plant-based principles). This paper is primarily concerned with the biomedical implications of lead-induced generation of free radical and the toxicity management in the mammalian system.

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“…[12]. It is a free radical scavenger and a membrane stabilizer that prevents lipoperoxidation and reduced glutathione depletion in some experimental models [13]. It has been also reported that having multiple pharmacological activities including hepatoprotectant, an anti-inflammatory agent, antibacterial, anti-allergic, antiviral, anti mutagenic, antineoplastic, and antithrombotic agent [14].…”

Section: Introductionmentioning

confidence: 99%

Effect of Silymarin Extracted From Silybum Marianum on Nickel Hematotoxicity and Nephrotoxicity in Male Albino Wistar Rats

Bouhalit

Kechrid

Elfeki

2017

Int J Pharm Pharm Sci

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Objective: The objective of this study was to investigate the effect of silymarin extract from Silybum marianum against nickel-induced alterations in haematological indices, kidney dysfunction and renal antioxidant defence system. Methods:Male albino Wistar rats were divided into four groups seven each. Control, silymarin, nickel and nickel plus silymarin. Silymarin was administrated orally (100 mg/kg b. wt) and nickel as nickel sulfate (NiSO4 6H2 Results:The treatment with nickel led to a significant decrease in body weight with an increase in both absolute and relative kidney weights and a significant increase in renal markers, which confirmed by histopathological alteration. A microcytic anemia was also observed, which was manifested by a reduction of red blood cells count (RBC), hemoglobin (Hb) concentration, platelet counts (Plt), hematocrit and white blood cells counts (WBC). The level of lipid peroxidation was increased. Whereas, GSH concentration and enzymatic antioxidants SOD, GSH-Px and CAT activities were decreased. The co-treatment with methanolic extract of milk thistle attenuated the variation in the hematological and renal markers, decreasing renal lipid peroxidation (p<0.05) with a concomitant increasing reduced glutathione content (p<0.01) and restoring the antioxidant enzymes (SOD, CAT, GSH-Px) in kidney, as well as an improvement in histological changes compared to those previously noticed in nickel group. 0) was given intraperitoneally (20 mg/kg b. wt) at alternative days. The experiment continued for three consecutive weeks. Body weight was recorded regularly. After overnight fasting, animals were killed and serum creatinine, serum urea, serum uric acid, hematological parameters and renal antioxidant markers were determined. Conclusion:To conclude, these findings demonstrated that silymarin extract effectively improved heamatotoxicity and nephrotoxicity caused by nickel.

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Comparative Effect of Silymarin and D-Penicillamine on Lead Induced Hemotoxicity and Oxidative Stress in Rat

Abstract: Background: This study was performed to investigate the adverse effects of acute lead

Cited by 8 publications

References 30 publications

Lead-induced increase in erythrocyte osmotic fragility and malondialdehyde concentration in Wistar rats: Chemo-protective effects of flavonoid mixture

Lead-induced increase in erythrocyte osmotic fragility and malondialdehyde concentration in Wistar rats: Chemo-protective effects of flavonoid mixture

Biochemical and Molecular Bases of Lead-Induced Toxicity in Mammalian Systems and Possible Mitigations

Effect of Silymarin Extracted From Silybum Marianum on Nickel Hematotoxicity and Nephrotoxicity in Male Albino Wistar Rats

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