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

Al Omar S. Yousef, Alkhuriji A. Fahad, Ahmed E. Abdel Moneim, Dina M. Metwally, Manal F. El-khadragy and Rami B. Kassab
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Al Omar S. Yousef: Zoology Department, Faculty of Science, King Saud University, Riyadh 11451, Saudi Arabia
Alkhuriji A. Fahad: Zoology Department, Faculty of Science, King Saud University, Riyadh 11451, Saudi Arabia
Ahmed E. Abdel Moneim: Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo 11795, Egypt
Dina M. Metwally: Zoology Department, Faculty of Science, King Saud University, Riyadh 11451, Saudi Arabia
Manal F. El-khadragy: Zoology Department, Faculty of Science, King Saud University, Riyadh 11451, Saudi Arabia
Rami B. Kassab: Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo 11795, Egypt

IJERPH, 2019, vol. 16, issue 16, 1-17

Abstract: 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 (CoQ 10 ) 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 CoQ 10 group was injected with CoQ 10 (10 mg/kg); PbAc group was injected with PbAc (20 mg/kg); PbAc + CoQ 10 group was injected first with PbAc, and after 1 h with CoQ 10 . 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 CoQ 10 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 CoQ 10 has beneficial effects against PbAc-induced neuronal damage through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activities.

Keywords: lead; coenzyme Q10; Nrf2/HO-1 pathway; inflammation; neurotransmission; apoptosis; brain (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2019
References: View complete reference list from CitEc
Citations: View citations in EconPapers (1)

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