Melatonin ameliorates oxidative damage induced by maternal lead exposure in rat pups

Bazrgar, Maryam; Goudarzi, Iran; Lashkarbolouki, Taghi; Salmani, Mahmoud Elahdadi

doi:10.1016/j.physbeh.2015.06.040

Cited by 37 publications

(16 citation statements)

References 83 publications

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“…Moreover; it reduced brain ammonia and NOx levels. These results are in rhyme with previous researches; where reduction of aggressive behavior and hyper locomotor activity by MLN as well as neuroprotective properties and amelioration of brain oxidative stress have been previously reported in other psychotic conditions (Bazrgar et al, 2015, Souza et al, 2014. The neuroprotective role of MLN is attributed to its ability to ameliorate radical formation through its anti-excitatory and anti-inflammatory effects (Pandi-Perumal et al, 2006).…”

Section: Discussionsupporting

confidence: 92%

Methionine and Choline Deficient Diet-induced Non-Alcoholic Steatohepatitis in Rats: Role of Melatonin

2017

J App Pharm Sci

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Objective: The present study aimed to evaluate the neuro-protective and hepato-protective activity of melatonin (MLN) on non-alcoholic steatohepatitis (NASH) in albino rats induced by methionine and choline deficient (MCD) diet. Material and Methods: To achieve this aim, rats were fed MCD diet for 8 weeks to induce non-alcoholic steatohepatitis. Oral administration of MLN (10 mg/kg/day) was done for the last two consecutive weeks. Twenty-four hours after the last dose of the MLN behavioral test, namely activity cage test was performed and the activity counts were recorded. Serum AST, ALT, ALP, GGT, total/direct bilirubin and albumin were valued to assess liver function. Moreover, hepatic interleukin-6 (IL-6) as well as nuclear factor-kβ (NF-kβ) were determined. Besides, brain biomarkers viz. ammonia, nitric oxide and brain-derived neurotrophic factor (BDNF) were measured which are reliable indices to assess brain damage. Results: MLN succeeded in suppression of NASH rats' locomotor activity. Besides; it improved all biochemical parameters and histopathological as well as proliferating cell nuclear antigen (PCNA) immunohistochemical profiles of liver and brain. Conclusions: These results afford new intuition into the possible molecular mechanisms by which MLN faces steatohepatitis disorder, via modulation of several factors participating in the progression of this disease.

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Section: Discussionsupporting

confidence: 92%

Methionine and Choline Deficient Diet-induced Non-Alcoholic Steatohepatitis in Rats: Role of Melatonin

2017

J App Pharm Sci

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“…In rats, the activities of GPX and SOD, as oxidative stress markers, significantly decreased in the Pb treatment group [34]. In human, the decreased activities of GPX and SOD were observed when treated by Pb[35].…”

Section: Discussionmentioning

confidence: 99%

Antagonistic effects of selenium on lead-induced autophagy by influencing mitochondrial dynamics in the spleen of chickens

Yang

et al. 2017

Oncotarget

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Lead (Pb) may damage the immune function in human and animal. Selenium (Se) has antagonistic effects on Pb. In our study, brown layer chickens were randomly allocated to control group, Se group (1 mg/kg Se), Se+Pb group (1 mg/kg Se and 350 mg/kg Pb), and Pb group (350 mg/kg Pb). The chickens were sacrificed on the 90th day; spleen tissues were subjected to observation of ultrastructure and detection of spleen-related indexes. The results revealed that in the Pb group, expression levels of the cytokines IL-1 and TNF-α significantly increased, and expression levels of IL-2 and INF-γ significantly decreased; activities of antioxidant enzyme GPX, SOD and CAT significantly decreased, and expression level of malondialdehyde (MDA) significantly increased; expression levels of mitochondrial fission-related genes (Mff and Drp1) significantly increased, and expression levels of mitochondrial fusion-related genes (Opa1, Mfn1 and Mfn2) significantly decreased; expression of autophagy-related genes (Beclin 1, Dynein, Atg 5, LC3-I and LC-II) was upregulated, while expression of mammalian target of rapamycin (mTOR) was downregulated. The results of transmission electron microscopy indicated that Pb induced mitochondrial fragmentation, and triggered autophagy in the spleen of chickens. The Se and Pb co-treatment remarkably alleviated these injuries induced by Pb in the spleen of chickens. In conclusion, Pb can induce the oxidative stress to influence the mitochondrial dynamics balance and lead to autophagy, which triggers the immune dysfunction in the spleen of chickens; the Se exhibits the antagonistic effects on lead-induced autophagy by influencing mitochondrial dynamics in the spleen of chickens.

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“…It is selectively deposited in these brain regions and found to be associated with behavioral abnormalities, learning impairment, decreased hearing, neuromuscular weakness and impaired cognitive functions in humans and in experimental animals [37] . It may also result in many biochemical alterations and a variety of neurological disorders, such as mental retardation, behavioral problems, nerve damage, Alzheimer's disease, schizophrenia and Parkinson's disease [38,39] . Studies have also reported the association of lead exposure to CNS damage and cause forgetfulness, irritability, poor attention span, headache, fatigue, impotence, dizziness and depression [40] .…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Singh

Yadav

et al. 2017

Ann Neurosci

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Background: Lead is widely distributed in the environment and has been found to be associated with various health problems including neurodegenerative diseases. Purpose: In view of the increasing health risk caused by lead, this study has been carried out to investigate the neuroprotective effect of omega-3 fatty acid (omega-3FA) in lead-induced neurotoxicity in rats. Methods: Biochemical parameters including oxidative stress in brain regions, lead levels in blood and brain regions and histopathological examination of brain regions of rats were carried out in the present study. Results: Rats exposed to lead (lead acetate 7.5 mg/kg body weight p.o. for 14 days) caused a significant increase in the levels of lipid peroxidation, protein carbonyl content, ROS production and decreased the activities of glutathione peroxidase, superoxide dismutase and catalase in the cerebellum and cerebral cortex, respectively, as compared to controls. Abnormal histopathological changes and increase in the levels of lead in blood and brain were also observed as compared to controls. Co-treatment of lead with omega-3FA (750 mg/kg body weight p.o. for 14 days) decreased the levels of lipid peroxidation, protein carbonyl content, ROS production and increased the activities of glutathione peroxidase, superoxide dismutase and catalase and showed protection in the histopathological study as compared to rats treated with lead alone. Conclusions: The result of the present study shows that lead-induced oxidative stress and histopathological alteration in the brain region were significantly protected with co-treatment of lead and omega-3FA. This could be due to its strong antioxidant potential and metal-binding property.

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Melatonin ameliorates oxidative damage induced by maternal lead exposure in rat pups

Cited by 37 publications

References 83 publications

Methionine and Choline Deficient Diet-induced Non-Alcoholic Steatohepatitis in Rats: Role of Melatonin

Methionine and Choline Deficient Diet-induced Non-Alcoholic Steatohepatitis in Rats: Role of Melatonin

Antagonistic effects of selenium on lead-induced autophagy by influencing mitochondrial dynamics in the spleen of chickens

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

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