Abhishek Kumar1, Nikhat J Siddiqi2, Sara T Alrashood3, Haseeb A Khan2, Anchal Dubey1, Bechan Sharma4. 1. Department of Biochemistry, University of Allahabad, Allahabad 211002, India. 2. Department of Biochemistry, College of Science, King Saud University, Riyadh 11495, Saudi Arabia. 3. Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia. 4. Department of Biochemistry, University of Allahabad, Allahabad 211002, India. Electronic address: sharmabi@yahoo.com.
Abstract
BACKGROUND: Cadmium is one of the most toxic heavy metals. The prolonged exposure of it can lead to severe alterations and damage in different tissues including blood, liver, kidney and brain. Eugenol, a phenolic compound, is present in various aromatic plants. It acts as a natural antioxidant and anti-inflammatory agent. The aim of this study was to investigate whether the treatment of eugenol is beneficial against the hepatic oxidative stress and inflammation induced by Cd. METHODS: To study the effect of eugenol in reversal of Cd toxicity, 24 albino rats were equally divided into four different groups: G1 Control (saline), G2 Eugenol (3 mg kg-1), G3 CdCl2 (5 mg kg-1) and G4 CdCl2 + Eugenol (5 mg kg-1 + 3 mg kg-1). All the groups were treated with gavage orally for the period of 21 days. After this treatment period, rats were sacrificed and liver tissues were removed. The hepatic antioxidant status was evaluated by measuring the activities of SOD, Catalase and GST enzymes. The reduced glutathione, lipid peroxidation, protein carbonyl oxidation (PCO) and thiol contents were measured in hepatic tissues. The activities of liver marker enzymes such as ALT, AST, GGT, ALP, TP, albumin, Bilirubin content and LDH were determined to assess the hepatic damage in different groups. Cd induced hepatic inflammation was determined by evaluating the levels of TNF-a, IL-6 and NO. RESULTS: Oral intoxication of Cd for 21 days significantly elevated the level of hepatic markers including activities of LDH, GGT, ALP, ALT, AST and Bilirubin level. The albumin content, reduced GSH level, and activities of antioxidant enzymes were significantly reduced in Cd treated group. The levels of inflammatory markers were significantly elevated in Cd treated group. The eugenol treatment was very effective and it significantly reversed the Cd induced biochemical alterations almost similar to that of control. CONCLUSION: The results demonstrated that the eugenol possessed very strong anti-oxidative and anti-inflammatory potential. The co-treatment of eugenol with Cd exhibited protective potential of eugenol against Cd induced toxicity. Eugenol was able to improve the cellular redox system in rats treated with Cd.
BACKGROUND:Cadmium is one of the most toxic heavy metals. The prolonged exposure of it can lead to severe alterations and damage in different tissues including blood, liver, kidney and brain. Eugenol, a phenolic compound, is present in various aromatic plants. It acts as a natural antioxidant and anti-inflammatory agent. The aim of this study was to investigate whether the treatment of eugenol is beneficial against the hepatic oxidative stress and inflammation induced by Cd. METHODS: To study the effect of eugenol in reversal of Cdtoxicity, 24 albino rats were equally divided into four different groups: G1 Control (saline), G2 Eugenol (3 mg kg-1), G3 CdCl2 (5 mg kg-1) and G4 CdCl2 + Eugenol (5 mg kg-1 + 3 mg kg-1). All the groups were treated with gavage orally for the period of 21 days. After this treatment period, rats were sacrificed and liver tissues were removed. The hepatic antioxidant status was evaluated by measuring the activities of SOD, Catalase and GST enzymes. The reduced glutathione, lipid peroxidation, protein carbonyl oxidation (PCO) and thiol contents were measured in hepatic tissues. The activities of liver marker enzymes such as ALT, AST, GGT, ALP, TP, albumin, Bilirubin content and LDH were determined to assess the hepatic damage in different groups. Cd induced hepatic inflammation was determined by evaluating the levels of TNF-a, IL-6 and NO. RESULTS: Oral intoxication of Cd for 21 days significantly elevated the level of hepatic markers including activities of LDH, GGT, ALP, ALT, AST and Bilirubin level. The albumin content, reduced GSH level, and activities of antioxidant enzymes were significantly reduced in Cd treated group. The levels of inflammatory markers were significantly elevated in Cd treated group. The eugenol treatment was very effective and it significantly reversed the Cd induced biochemical alterations almost similar to that of control. CONCLUSION: The results demonstrated that the eugenol possessed very strong anti-oxidative and anti-inflammatory potential. The co-treatment of eugenol with Cd exhibited protective potential of eugenol against Cd induced toxicity. Eugenol was able to improve the cellular redox system in rats treated with Cd.
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