Coenzyme Q10 Activates the Antioxidant Machinery and Inhibits the Inflammatory and Apoptotic Cascades Against Lead Acetate-Induced Renal Injury in Rats

Abstract

The kidney is among the metabolic organs most susceptible to injury, particularly following exposure to xenobiotics and heavy metals. We aimed to explore the potential protective impacts of coenzyme Q10 (CoQ10) on lead acetate (PbAc)-induced nephrotoxicity in rats. Four experimental groups (n = 7) were applied as follows: control group, CoQ10 alone (10 mg/kg), PbAc alone (20 mg/kg), and PbAc with CoQ10. Exposure to PbAc led to the accumulation of Pb in the kidney and increased urea and creatinine serum levels. The deposition of Pb coupled with the elevation of malondialdehyde and nitrate/nitrite levels along with the upregulation of inducible nitric oxide synthase. Additionally, upon PbAc poisoning, glutathione content and the antioxidant enzymes were depleted along with the downregulation of Nrf2 and HO-1 expression. Moreover, PbAc injection increased the protein and mRNA levels of pro-inflammatory cytokines namely, tumor necrosis factor-alpha and interleukin-1 beta, while decreased the levels of interleukin-10, an anti-inflammatory cytokine, in the kidney. Furthermore, exposure to PbAc correlated with increased levels of pro-apoptotic markers, Bax and caspase-3, and reduced levels of the anti-apoptotic marker Bcl-2. The administration of CoQ10 alleviated the molecular, biochemical and histological changes following PbAc intoxication. Thus, CoQ10 reduces the deleterious cellular side effects of PbAc exposure due to its antioxidant, anti-inflammatory and anti-apoptotic effects.

Moringa oleifera Lam. extract rescues lead‐induced oxidative stress, inflammation, and apoptosis in the rat cerebral cortex

“…Lead has a high affinity for thiol groups or metal cofactors in enzymatic and non‐enzymatic antioxidants and molecules, the binding of which results in a decline in antioxidant enzyme activities, including SOD, CAT, GPx, and GR activities (Baty et al., 2020). Our experimental findings are in accordance with those of AL‐Megrin, Soliman, et al (2020), who reported a prominent elevation in hepatic MDA levels and a marked depletion in enzymatic and non‐enzymatic antioxidants and molecules. SOD, CAT, and GPx form the first line of defense against ROS, and decrease in their activities contributes to oxidative stress in tissues.…”

“…CAT and SOD are important antioxidant agent catalysts that play critical roles in the removal of superoxide from the natural framework. Pb can supplant zinc and other significant cofactor metals, leading to the loss of a protective antioxidant response in addition to lowering GSH activity (AL‐Megrin, Soliman, et al, 2020). Curiously, MOE treatment forestalls oxidative stress, indicating its remarkable protective effect in cortical tissue.…”

“…Lead (Pb), a toxic heavy metal, is often used in the production and recycling of batteries, petrol, and paints (AL‐Megrin, Alkhuriji, et al, 2020; AL‐Megrin, Soliman, et al, 2020). According to Obeng‐Gyasi et al.…”

Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

“…3 To date, several endogenous free radical scavengers (including enzymatic factors such as catalase, superoxide dismutase (SOD), and selenium and / or non-selenium-dependent glutathione peroxidase (GPx) and nonenzymatic scavengers, such as glutathione (GSH); bilirubin; albumin; vitamins A, E, and C; selenium, uric acid, and coenzyme Q-10, have been identified in both the membranes and cytoplasm of cells. 8 Arsenic induces oxidative pressure through excessive overproduction of reactive oxygen and nitrogen species (ROS/RNS), depletion of the antioxidant capacity of cells, 5 and suppression of DNA repair mechanisms. 2 Arsenic also depletes the cellular concentrations of both enzymatic and nonenzymatic molecules.…”

Liposome/gold hybrid nanoparticle encoded with CoQ10 (LGNP-CoQ10) suppressed rheumatoid arthritis via STAT3/Th17 targeting

“…In mitochondria, CoQ10 plays a critical role in producing adenosine triphosphate (ATP) via the oxidative phosphorylation pathway [9,10]. Recently, CoQ10 has been reported to have anti-inflammatory functions and exhibit therapeutic effects for immune disorders [11,12]. Some studies have demonstrated therapeutic effects of CoQ10 against RA through the regulation of immune process factors such as tumor necrosis factor (TNF)-α and IL-6 [13,14].…”