Protocatechuic acid mitigates cadmium-induced neurotoxicity in rats: Role of oxidative stress, inflammation and apoptosis

Olayan, Ebtesam M. Al; Aloufi, Abeer S.; Alamri, Ohoud; El-Habit, Ola H.; Moneim, Ahmed E. Abdel

doi:10.1016/j.scitotenv.2020.137969

Cited by 125 publications

(59 citation statements)

References 57 publications

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“…Increased ROS levels are attributed to mitochondrial hyperactivity, electron leakage, and enhanced electron transport chain activity. Indeed, ROS attacks almost all cellular components, including membrane phospholipids, and causes LPO [ 27 ]. As another possible mechanism, Pérez et al [ 28 ] hypothesized that the toxic effects of Al are mediated by damage to cell membranes.…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

Othman

Fareid

Hameed

et al. 2020

Oxidative Medicine and Cellular Longevity

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Aluminum (Al) is a ubiquitous element with known toxicity for both humans and animals. Herein, we aimed to investigate the potential role of melatonin (MEL) in hepatotoxicity and nephrotoxicity following aluminum chloride (AlCl3) treatment in rats. Adult male rats were treated with AlCl3 (34 mg/kg bwt) for eight weeks. Exposure to AlCl3 enhanced the serum activities of the liver transaminases (alanine aminotransferase and aspartate aminotransferase) and increased the level of bilirubin, in addition to the serum kidney function markers urea and creatinine. AlCl3 intoxication boosted oxidative stress, as evidenced by increases in the levels of lipid peroxidation (LPO) and nitric oxide (NO) along with simultaneous decreases in the levels of glutathione (GSH), various antioxidant enzymes, and Nrf2 mRNA expression. MEL (5 mg/kg bwt) treatment repressed LPO and NO levels, whereas it augmented GSH content. The activities of the antioxidant enzymes GPx, SOD, CAT, and GR were also restored concomitantly when MEL was administered before AlCl3. MEL also suppressed the apoptotic effect of AlCl3 by enhancing Bcl-2 protein expression in the liver and kidney and decreasing the expression levels of proinflammatory cytokines. Histopathological findings in the liver and kidney tissues confirmed the beneficial effect of MEL against AlCl3 toxicity. These findings indicate that MEL prevents AlCl3 toxicity by enhancing the antioxidant defense system.

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Section: Discussionmentioning

confidence: 99%

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

Othman

Fareid

Hameed

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Although Cd cannot be considered as a redox‐active metal as it has not the ability of ROS generation itself by the Fenton‐like reactions, Cd binds to sulfhydryl (‐SH) groups of the ROS scavenging proteins and non‐proteins molecules like GSH that leading to indirect increase in ROS and oxidative stress, evidenced by lipid peroxidation and cell death (Olayan et al., 2020). In addition to GSH depletion, Cd can interact with the enzyme protein structure causing inactivation in its catalytic activity and replace the other divalent cation necessary for the antioxidant enzymes activity (Almeer, Soliman, et al., 2018).…”

Section: Discussionmentioning

confidence: 99%

Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium‐induced oxidative challenge, inflammation, and apoptosis in rats

et al. 2020

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Here, we examined the protective effect of ferulic acid (FA) on cadmium chloride (CdCl 2)-mediated reproductive toxicity in male rats. Animals were divided into four groups: control, FA (20 mg/kg), CdCl 2 (6.5 mg/kg), and FA + CdCl 2. CdCl 2 treatment evoked a significant increase in testis cadmium concentration in addition to obvious increase in testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Moreover, CdCl 2-induced oxidative damage through exhausting the cellular defenses (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) and downregulating the nuclear factor erythroid 2-related factor 2 (Nrf2) expression accompanied by increases of malondialdehyde and nitric oxide contents. Testicular inflammation was evident indicated by increased levels of interleukin-1β and tumor necrosis factor-α in CdCl 2-treated rats. CdCl 2 exposure also decreased the expression of the proliferating cell nuclear antigen and augmented apoptotic events associated with prominent histopathological alterations. However, FA coadministration mitigated the impaired hormonal level, apoptotic and inflammatory injuries elicited by CdCl 2, and maintained the oxidant/antioxidant balance in testicular tissue via Nrf2 activation. Practical applications Cadmium is an environmental toxicant and known to cause adverse effects including reproductive toxicity. However, antioxidant application has been found to protect against heavy metals-mediated toxic effects. Here, we examined the potential protective efficacy of ferulic acid against cadmium-mediated testicular impairments through estimating the amount of cadmium in the testis, hormonal profile, oxidative status, inflammatory response, apoptotic and proliferating markers in addition to the histopathological alterations. The obtained findings revealed that ferulic acid supplementation was able to abolish the testicular damages coupled with cadmium exposure. The protective efficiency of ferulic acid may correlated with its strong antioxidant, anti-inflammatory, and antiapoptotic activities; suggesting that ferulic acid may be used to ameliorate cadmium-induced testicular deficits. How to cite this article: Kassab RB, Lokman MS, Daabo HMA, et al. Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium-induced oxidative challenge, inflammation, and apoptosis in rats.

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“…Hydrogen peroxide decomposition is effectively promoted by CAT, which consequently prevents lipid peroxidation (Albasher et al., 2020). GSH and GPx catalyze the decline of lipid peroxides and H 2 O 2 (hydrogen peroxide), while GR advances the NADPH‐driven reduction of oxidized GSH (Al Olayan et al., 2020). Depletion of these antioxidants and particles could lead to an accumulation of hydrogen peroxide, which can disrupt neuronal cell integrity (Mohamed et al., 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have demonstrated that MOE contributed to cancer prevention by deactivating NO and MDA, and improving non‐enzymatic and enzymatic antioxidant activities. Flavonoids and polyphenols are hydrogen molecule donors that can eliminate free radicals and protect mammalian cells from ROS‐induced damage (Al Olayan et al., 2020). The capacity of MOE to improve glutathione accumulation and other protective enzymes has been well documented.…”

Section: Discussionmentioning

confidence: 99%

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

Al-Qahtani

Albasher

2020

J. Food Biochem.

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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. (2018) and Qi et al. (2019), exposure to Pb affects the central nervous system and the hematopoietic, hepatic, excretory, and reproductive systems, leading to serious dysfunction. There are few reports on the safe levels of Pb. However, Mason et al. (2014) note that exposure to even low levels of Pb (5 μg/dl) may lead to reduced

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Protocatechuic acid mitigates cadmium-induced neurotoxicity in rats: Role of oxidative stress, inflammation and apoptosis

Cited by 125 publications

References 57 publications

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium‐induced oxidative challenge, inflammation, and apoptosis in rats

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

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