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Open AccessArticle

The Neuroprotective Role of Coenzyme Q10 Against Lead Acetate-Induced Neurotoxicity Is Mediated by Antioxidant, Anti-Inflammatory and Anti-Apoptotic Activities

Zoology Department, Faculty of Science, King Saud University, Riyadh 11451, Saudi Arabia
Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo 11795, Egypt
Parasitology Department, Faculty of Veterinary Medicine, Zagazig University, Zagazig 12878, Egypt
Author to whom correspondence should be addressed.
Int. J. Environ. Res. Public Health 2019, 16(16), 2895;
Received: 21 May 2019 / Revised: 16 July 2019 / Accepted: 18 July 2019 / Published: 13 August 2019
(This article belongs to the Special Issue Metal Exposure and Health Risk Assessment)
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Heavy metal exposure, in lead (Pb) particularly, is associated with severe neuronal impairment though oxidative stress mediated by reactive oxygen species, and antioxidants may be used to abolish these adverse effects. This study investigated the potential neuroprotective role of coenzyme Q10 (CoQ10) against lead acetate (PbAc)-induced neurotoxicity. Twenty-eight male Wistar albino rats were divided into four equal groups (n = 7) and treated as follows: the control group was injected with physiological saline (0.9% NaCl); the CoQ10 group was injected with CoQ10 (10 mg/kg); PbAc group was injected with PbAc (20 mg/kg); PbAc + CoQ10 group was injected first with PbAc, and after 1 h with CoQ10. All groups were injected intraperitoneally for seven days. PbAc significantly increased cortical lipid peroxidation, nitrate/nitrite levels, and inducible nitric oxide synthase expression, and decreased glutathione content, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activity and mRNA expression, as well as nuclear factor erythroid 2–related factor 2 (Nrf2) and homoxygenase-1 (HO-1) expression. PbAc also promoted the secretion of interleukin-1ß and tumor necrosis factor-α, inhibited interleukin-10 production, triggered the activation of pro-apoptotic proteins, and suppressed anti-apoptotic proteins. Additionally, PbAc increased the cortical levels of serotonin, dopamine, norepinephrine, GABA, and glutamate, and decreased the level of ATP. However, treatment with CoQ10 rescued cortical neurons from PbAc-induced neurotoxicity by restoring the balance between oxidants and antioxidants, activating the Nrf2/HO-1 pathway, suppressing inflammation, inhibiting the apoptotic cascade, and modulating cortical neurotransmission and energy metabolism. Altogether, our findings indicate that CoQ10 has beneficial effects against PbAc-induced neuronal damage through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activities. View Full-Text
Keywords: lead; coenzyme Q10; Nrf2/HO-1 pathway; inflammation; neurotransmission; apoptosis; brain lead; coenzyme Q10; Nrf2/HO-1 pathway; inflammation; neurotransmission; apoptosis; brain

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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S. Yousef, A.O.; A. Fahad, A.; Abdel Moneim, A.E.; Metwally, D.M.; El-khadragy, M.F.; Kassab, R.B. The Neuroprotective Role of Coenzyme Q10 Against Lead Acetate-Induced Neurotoxicity Is Mediated by Antioxidant, Anti-Inflammatory and Anti-Apoptotic Activities. Int. J. Environ. Res. Public Health 2019, 16, 2895.

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