Lead-induced oxidative damage in rats/mice: A meta-analysis

Fan, Yongsheng; Zhao, Xue; Yu, Jun; Xie, Jie; Liu, Cong; Liu, Duanya; Tang, Caoli; Wang, Chunhong

doi:10.1016/j.jtemb.2019.126443

Cited by 61 publications

(27 citation statements)

References 37 publications

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“…GSH is one of the cellular antioxidants used to detoxify peroxides and various electrophilic compounds using GST and GPX. In addition, GSH neutralized the radicals-generated from Pb metabolism and make chelation and detoxification of it [3]. By accumulating Pb and increasing the Pb level over time, this will cause exhaustion of the antioxidant enzymes including SOD, catalase, and GPX.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, these enzymes have been inactivated by Pb due to inhibition of their functional -SH groups. Also, Pb can chelate selenium, which is an important cofactor for GPX activity [3]. The GST activity decreased after Pb administration that may be owed to increase the production of peroxides after Pb metabolism that leads to exhaustion of the enzyme.…”

Section: Discussionmentioning

confidence: 99%

“…Hepatotoxicity can also be induced by natural chemical agents (such as aflatoxin), industrial agents, and heavy metals (such as lead, Pb) [2]. The Pb is a toxic heavy metal with a wide abundance in the earthand it can be absorbed via the respiratory system, gastrointestinal tracts, and rarely through the skin [3]. After absorption, Pb is distributed in the blood, bone, and soft tissues, while the liver is the main storehouse (33%).…”

Section: Introductionmentioning

confidence: 99%

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The synergistic hepatoprotective potential of Beta vulgaris juice and 2,3- dimercaptosuccinic acid in lead-intoxicated rats via improving the hepatic oxidative and inflammatory stress

Shaban

Abdelrahman

Elkersh

et al. 2020

BMC Complement Med Ther

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Background: Lead (Pb) is observed in all areas of the environment, mainly derived from human operations such as mining, processing, and burning fossil fuels. Pb toxicity is one of the most prevalent causes of human hepatotoxicity. The available chelator drugs used now have many adverse effects and therefore the world is looking for natural and secure alternatives. Methods: Here, we evaluated the hepatoprotective role of the oral administration (1 g/kg b.w.) of the lyophilized Beta vulgaris juice (BVJ) against Pb-induced rat hepatotoxicity. We also examined the possible synergistic hepatoprotective impact of the combination between BVJ and 2,3-dimercaptosuccinic acid (DMSA, the currently approved drug for Pbtoxicity). The evaluation depends on the ability of BVJ, DMSA, or their combination (BVJ-DMSA) to reduce serum and hepatic Pb level and to avoid oxidative stress and inflammation caused by Pb. The level of lipid peroxidation, reduced glutathione (GSH), total antioxidant capacity, and the activity of the antioxidant enzymes were quantified. In addition, the level of interleukin (IL)-6, nitric oxide (NO), DNA fragmentation, and liver histology were studied. Results: The results showed that BVJ contained considerable amounts of betalains, vitamin C, and various types of phenolic compounds. Therefore, BVJ displayed a significant (p < 0.05) preventive influence on the elevation of Pb levels in blood and liver as well as the hepatic DNA fragmentation. In addition, it significantly (p < 0.05) improved most of the studied antioxidant and inflammatory markers in the Pb-intoxicated rats. However, the combined extract (BVJ-DMSA) revealed synergistic (combination index < 1) activities in most of the tested parameters. The histopathological results verified the biochemical findings of this research.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The synergistic hepatoprotective potential of Beta vulgaris juice and 2,3- dimercaptosuccinic acid in lead-intoxicated rats via improving the hepatic oxidative and inflammatory stress

Shaban

Abdelrahman

Elkersh

et al. 2020

BMC Complement Med Ther

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“…Pb toxicity is correlated with inducing oxidative stress of organisms, leading to the inactivation of antioxidant enzymes (Zhang et al, 2014;Fan et al, 2020). Hence, to evaluate whether CGA, NCGA, and CCGA co-treatment ameliorated Pb-induced oxidative stress, we have assessed the mRNA expression of several genes related to oxidative stress (sod2, sod1, cat, gclm, gsto2, and gpx4a).…”

Section: Effect On the Expression Of Genes Related To Oxidative Stressmentioning

confidence: 99%

Protective Effect of Chlorogenic Acid and Its Analogues on Lead-Induced Developmental Neurotoxicity Through Modulating Oxidative Stress and Autophagy

Wang

Paudel

et al. 2021

Front. Mol. Biosci.

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Lead (Pb) is among the deleterious heavy metal and has caused global health concerns due to its tendency to cause a detrimental effect on the development of the central nervous system (CNS). Despite being a serious health concern, treatment of Pb poisoning is not yet available, reflecting the pressing need for compounds that can relieve Pb-induced toxicity, especially neurotoxicity. In the quest of exploring protective strategies against Pb-induced developmental neurotoxicity, compounds from natural resources have gained increased attention. Chlorogenic acid (CGA) and its analogues neochlorogenic acid (NCGA) and cryptochlorogenic acid (CCGA) are the important phenolic compounds widely distributed in plants. Herein, utilizing zebrafish as a model organism, we modeled Pb-induced developmental neurotoxicity and investigated the protective effect of CGA, NCGA, and CCGA co-treatment. In zebrafish, Pb exposure (1,000 μg/L) for 5 days causes developmental malformation, loss of dopaminergic (DA) neurons, and brain vasculature, as well as disrupted neuron differentiation in the CNS. Additionally, Pb-treated zebrafish exhibited abnormal locomotion. Notably, co-treatment with CGA (100 µM), NCGA (100 µM), and CCGA (50 µM) alleviated these developmental malformation and neurotoxicity induced by Pb. Further underlying mechanism investigation revealed that these dietary phenolic acid compounds may ameliorate Pb-induced oxidative stress and autophagy in zebrafish, therefore protecting against Pb-induced developmental neurotoxicity. In general, our study indicates that CGA, NCGA, and CCGA could be promising agents for treating neurotoxicity induced by Pb, and CCGA shows the strongest detoxifying activity.

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“…In the brain, particularly the developing brain, Pb can affect almost all of the processes critical to neuronal functions, such as pre-and post-synaptic functions, redox homeostasis, calcium regulation, protein homeostasis and signaling, epigenetics, genotoxicity and gene expression regulation, neuroinflammation, lipid metabolism, mitochondrial functions, and metabolism. Because there are several excellent reviews extensively describing the molecular and cellular aspects of Pb neurotoxicity, both alone [8,[123][124][125][126][127][128][129][130][131][132][133][134] and as a component of toxic metal mixtures [135][136][137], we do not attempt to summarize them again in this review.…”

Section: Molecular and Cellular Mechanisms Of Developmental Pb Neurotmentioning

confidence: 99%

(Ascorb)ing Pb Neurotoxicity in the Developing Brain

Ahmad

Liu

2020

Antioxidants

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Lead (Pb) neurotoxicity is a major concern, particularly in children. Developmental exposure to Pb can alter neurodevelopmental trajectory and has permanent neuropathological consequences, including an increased vulnerability to further stressors. Ascorbic acid is among most researched antioxidant nutrients and has a special role in maintaining redox homeostasis in physiological and physio-pathological brain states. Furthermore, because of its capacity to chelate metal ions, ascorbic acid may particularly serve as a potent therapeutic agent in Pb poisoning. The present review first discusses the major consequences of Pb exposure in children and then proceeds to present evidence from human and animal studies for ascorbic acid as an efficient ameliorative supplemental nutrient in Pb poisoning, with a particular focus on developmental Pb neurotoxicity. In doing so, it is hoped that there is a revitalization for further research on understanding the brain functions of this essential, safe, and readily available vitamin in physiological states, as well to justify and establish it as an effective neuroprotective and modulatory factor in the pathologies of the nervous system, including developmental neuropathologies.

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Lead-induced oxidative damage in rats/mice: A meta-analysis

Cited by 61 publications

References 37 publications

The synergistic hepatoprotective potential of Beta vulgaris juice and 2,3- dimercaptosuccinic acid in lead-intoxicated rats via improving the hepatic oxidative and inflammatory stress

The synergistic hepatoprotective potential of Beta vulgaris juice and 2,3- dimercaptosuccinic acid in lead-intoxicated rats via improving the hepatic oxidative and inflammatory stress

Protective Effect of Chlorogenic Acid and Its Analogues on Lead-Induced Developmental Neurotoxicity Through Modulating Oxidative Stress and Autophagy

(Ascorb)ing Pb Neurotoxicity in the Developing Brain

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