In Vivo Hepatoprotective Effect of Caffeic Acid on Mercuric Chloride-Induced Biochemical Changes in Albino Wistar Rats

Abstract

Objective: Mercury (Hg) is a highly dangerous and also one of the harmful heavy metals which induces oxidative stress in the animal body. The present study is planned to examine the possible defensive result of caffeic acid (CA) against mercury chloride (HgCl2)-induced hepatotoxicity in male albino Wistar rats, Rattus norvegicus.
 Methods: Sublethal dose of HgCl2 (1.29 mg/kg body weight) was administrated in rats for 15 days through oral dose and the CA was administrated for another 15 days on mercuric-intoxicated rats. After completing the scheduled exposure time, the rats were sacrificed and the whole liver organ was removed immediately from the animal, and it was used to carry out for biochemical and bioenzymological studies to observe.
 Results: The level of lipid peroxidation (LPO) content reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the liver tissue. CA is an energetic component in the phenolic propolis extract and also in a wide variety of plants, and a strong antioxidant helps to prevent oxidative damage and to reduce oxidative stress. The antioxidants such as GPx, CAT, and SOD and non-antioxidant GSH were significantly decreased, and also, the LPO level was increased in mercury toxicity rats. The treatment of CA (5 mg/kg body weight) in the liver tissue shows considerable declining in the level of oxidant content and along with an increase in the level of antioxidant properties by the way of improvement in liver tissues. Antioxidant and non-antioxidant enzyme (LOP, GSH, GPx, SOD, and CAT) activities were also significantly decreased to near untreated control level when compared to Hg-treated group. The CA acid alone treatment showed the enhanced antioxidant levels and not any alteration in the levels of biochemical parameters when compared with control.
 Conclusion: These observations of the present experimental study clearly explained the detoxify effects and protective effect of CA against HgCl2 toxicity in liver tissue.

Therapeutic potential of caffeic acid and coumarin in modifying aluminum-induced hepatic injury in Wistar rats

“…This is indicated by the levels of TBARS, carbonyls, and NO, as well as the increased activities of antioxidant enzymes (CAT, SOD, GP-x) in the Al-CA and Al-Coum groups compared to the Al group. These outcomes are consistent with those of previous reports by Bilgin et al (2011), Rajarajeswari andPari (2011), Olayinka et al (2017), and Manju and Jagadeesan (2019), which showed that caffeic acid and coumarin can scavenge free radicals and enhance the activities of antioxidant enzymes by decreasing oxidative stress. Particularly, Rajarajeswari and Pari (2011) found that coumarin restores peroxidative lipid markers to normal levels in diabetic rats, and Chang et al (1996) demonstrated its inhibition of lipoxygenase activity and lipid peroxidation and trapping of superoxide and hydroxyl radicals.…”

Ameliorative Effect of n-Butanol Fraction of Phoenix dactylifera on Mercury Induced Nephrotoxicity in Wistar Rats

“…Relative to oxidative stress bio-markers, it was noted that HgCl 2 diminished the activities of enzymatic antioxidants such as SOD and CAT (with a remarkable decline in CAT activity) in kidney tissues, whereas oxidative stress biomarkers (MDA contents) which is the end product of lipid peroxidation was increased compared to the control group. These ndings are in agreement with the reports of Manju and Jagadeesan 48 and Nabil et al 49 who implied that high accumulation of toxic metabolites in the system resulted from HgCl 2 -induced oxidative stress. Goudarzi et al 50 equally documented the reduction of antioxidant enzymes as a result of exposure to environmental toxins.…”

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“…The toxic dose of mercuric chloride has been resolved (sub-lethal dosage of HgCl 2 1.29 mg/kg body weight) from our past examination conducted in our laboratory. Furthermore, it has adequate to evoke gentle or mediated oxidative stress in rodents 36 .…”