Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar rats

Omobowale, Temidayo Olutayo; Oyagbemi, Ademola Adetokunbo; Akinrinde, Akinleye Stephen; Saba, Adebowale Benard; Daramola, Oluwabusola T.; Ogunpolu, Blessing Seun; Olopade, James Olukayode

doi:10.1016/j.etap.2014.03.002

Cited by 86 publications

(56 citation statements)

References 33 publications

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“…However, it was effectively alleviated in response to d-penicillamine or silymarin treatments. Similar results were reported by other researchers who observed a positive correlation between erythrocyte MDA levels and blood Pb levels [5,[33][34][35].…”

Section: Discussionsupporting

confidence: 80%

“…Higher levels of exposure to Pb in experimental or cross-Volume 11, No 3, May-June2017; http://www.ijt.ir sectional studies are reported to cause increases in the activity of these enzymes as a consequence of elevated reactive oxygen species production [3,[31][32]. However, the activities of GPx, CAT and SOD as major antioxidant enzymes in the erythrocytes significantly crashed usually at chronic exposure with lower amounts of lead [33]. Lead has the ability to bind to the sulfhydryl group of enzymes of the antioxidative defense system, as well as replacing divalent bioelements that serve as their important co-factors, resulting in their inactivation [3,[33][34].…”

Section: Discussionmentioning

confidence: 99%

“…However, the activities of GPx, CAT and SOD as major antioxidant enzymes in the erythrocytes significantly crashed usually at chronic exposure with lower amounts of lead [33]. Lead has the ability to bind to the sulfhydryl group of enzymes of the antioxidative defense system, as well as replacing divalent bioelements that serve as their important co-factors, resulting in their inactivation [3,[33][34].…”

Section: Discussionmentioning

confidence: 99%

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

Jalali

Najafzadeh

Mousavi

2017

IJT

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Jalali

Najafzadeh

Mousavi

2017

IJT

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“…Additionally, the markers of liver function remained persistently high, particularly AST, at early exposure periods in rats treated with PbAc, which may be indicative of hepatic damage (Omobowale et al, 2014). GE initially improved transaminases activities (Farag et al, 2010) but failed to restore their activity to normal towards the end of the exposure period.…”

Section: Discussionmentioning

confidence: 99%

Ginger extract modulates Pb-induced hepatic oxidative stress and expression of antioxidant gene transcripts in rat liver

Mohamed¹,

El‐Nahas

El‐Sayed

et al. 2015

Pharmaceutical Biology

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Context: Spices and herbs are recognized sources of natural antioxidants that can protect from oxidative stress, thus play an important role in chemoprevention of liver diseases. Ginger is used worldwide primarily as a spicy condiment. Objective: This study evaluated the ability of ginger extract (GE) to ameliorate oxidative-hepatic toxicity induced by lead acetate (PbAc) in rats. Materials and methods: Five groups of animals were used: group I kept as control; groups II, IV, and V received PbAc (1 ppm in drinking water daily for 6 weeks, and kept for an additional 2 weeks without PbAc exposure); group III treated orally with GE (350 mg/kg body weight, 4 d per week) for 6 weeks; group IV (protective) received GE for 2 weeks before and simultaneously with PbAc; and group V (treatment) received GE for 2 weeks after PbAc exposure. Results: GC-MS analysis of GE revealed its content of gingerol (7.09%), quercetin (3.20%), DL-limonene (0.96%), and zingiberene (0.18%). Treatment of PbAc-treated rats with GE has no effect on hepatic Pb concentrations. However, it maintained serum aspartate aminotransferase level, increased hepatic glutathione (157%), glutathione S-transferase (GST) (228%), glutathione peroxidase (GPx) (138%) and catalase (CAT) (112%) levels, and reduced hepatic malondialdehyde (80%). Co-treatment of PbAc group with GE upregulated mRNA expression of antioxidant genes: GST-a1 (1.4-fold), GPx1 (1.8-fold), and CAT (8-fold), while post-treatment with GE upregulated only mRNA expression of GPx1 (1.5-fold). Conclusion: GE has an antioxidant protective efficacy against PbAc-induced hepatotoxicity, which appears more effective than its therapeutic application. However, the changes in antioxidant gene expression were not reflected at the protein level.

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“…[16]. Superoxide dismutase was determined by measuring the inhibition of auto-oxidation of epinephrine at pH 10.2 as described by Misra & Fridovich [17] and with modification from our laboratory [18], [19]. The MDA level was calculated as described by Varshney & Kale [20].…”

Section: Methodsmentioning

confidence: 99%

Polyphenol-rich fraction of Parquetina nigrescens mitigates dichlorvos-induced neurotoxicity and apoptosis

Ochigbo

Saba

Oyagbemi

et al. 2017

Journal of Ayurveda and Integrative Medicine

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BackgroundParquetina nigrescens (Afzel.) Bullock of the family Asclepiadaceae is known for its antioxidant effects with wide range of uses in Southwestern Nigeria especially in traditional medicine. This study was undertaken to explore if polyphenol-rich fraction (prf) from P. nigrescens will ameliorate dichlorvos-induced neurotoxicity and apoptosis. The exploration utilized evaluation of markers of oxidative stress, apoptosis and serum acetylcholinesterase (AchE) levels.MethodsForty Wistar rats randomly placed in four groups were utilized for the study. Animals in Group A received corn oil, group B- dichlorvos (16 mg/kg), groups C and D- dichlorvos + 100 and 200 mg/kg prf of P. nigrescens respectively. Markers of oxidative stress, antioxidants and apoptosis were assessed in the serum and brain tissues using biochemical assay and immunohistochemistry.ResultsExposure to dichlorvos caused significant decreases in AchE, catalase, superoxide dismutase, glutathione peroxidase (GPx) and increases in hydrogen peroxide (H2O2) generation and malondialdehyde levels. Histopathology and immunohistochemistry of the cerebellum and cerebrum of rats exposed to dichlorvos revealed greater neurotoxic effects in the cerebellum as well as decreased expressions of AchE with a concomitant increase in Bax (proapototic) compared to prf of P. nigrescens treated rats.ConclusionThis study showed that dichlorvos caused cellular and tissue neurotoxicity by inhibiting AchE activity, induced oxidative stress and apoptosis in rats with prominent effects on the cerebellum than cerebrum. The prf of P. nigrescens showed amelioration of neurotoxicity by its antioxidative and antiapoptotic properties in rats exposed to dichlorvos.

show abstract

Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar rats

Cited by 86 publications

References 33 publications

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

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

Ginger extract modulates Pb-induced hepatic oxidative stress and expression of antioxidant gene transcripts in rat liver

Polyphenol-rich fraction of Parquetina nigrescens mitigates dichlorvos-induced neurotoxicity and apoptosis

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