Protective effect of cinnamon against cadmium-induced hepatorenal oxidative damage in rats

Abstract

Background: Cadmium (Cd) is a well-known hazardous environmental contaminant. It exerts its toxicity through induction of lipid peroxidation and reduction of cellular antioxidant. Therefore, in this study, we investigated whether cinnamon could protect against Cd toxicity in liver and kidney. Materials and methods: Forty male Wister rats (130-135 gm) were divided randomly into 4 groups/ 10 rats each. Control, cinnamon, cadmium, and Cinn+Cd groups received distilled water, cinnamon extract (200 mg/kg b.wt. orally), cadmium chloride (5 mg/kg b.wt. orally), and Cd plus cinnamon, respectively. Blood, liver, and kidney samples were collected after 8 weeks of treatment. Erythrogram, leukogram, liver and kidney functions, and oxidative status (MDA, CAT, and TAC) were determined. Results and discussion: Cd-treated animals showed significant increases in serum ALT, AST, creatinine, and urea indicating hepatic and renal damage. Cd-induced oxidative stress was observed by marked decease TAC accompanied by increase in MDA which contributed in liver and kidney dysfunction. Co-treatment of Cd with cinnamon has improved the oxidation profile by increasing the TAC and decreasing the lipid peroxidation. Cinnamon ameliorated the toxic effect of Cd, which observed by improvement of liver and kidney functions. Conclusion: High antioxidants content of cinnamon could protect the liver and kidney from Cd toxicity.

Coenzyme Q10 supplementation mitigates piroxicam-induced oxidative injury and apoptotic pathways in the stomach, liver, and kidney

“…6 ) compared to other kidney regions. These findings support our previous work, in which the cortex showed more damage due to oxidative stress in animal models of PM toxicity [ 7 , 35 ], acetaminophen [ 56 ], puromycin [ 57 ], gentamicin [ 58 ], cadmium [ 44 ], and mercury [ 59 ]. Taken all together, we strongly suggest that the overwhelming toxic effect of PM was mainly associated with mitochondrial dysfunction.…”

“…These events lead to massive necrosis of the liver and disturbances of liver function, as indicated in our study by a considerable decline in serum albumin and, consequently, total protein content. Impaired tubular reabsorption was another possible reason for the increased protein loss [ 43 , 44 ]. Likewise, this could be due to gastric ulceration and bleeding that resulted in malabsorption and decreased nourishment intake [ 5 ].…”

Cinnamon oil against acetaminophen-induced acute liver toxicity by attenuating inflammation, oxidative stress and apoptosis

“…Whereas CO treatment defenses liver injury by its scavenging property and improving antioxidant enzyme status in the liver. APAP mediated membrane damage is through the destruction of membrane lipids and oxidation of membrane proteins, collectively with APAP-induced mitochondrial disorder lead to impairment of tubular feature indicated by impaired uptake of albumin and proteins [ 38 , 39 ].…”

Piperine Enhances the Antioxidant and Anti-Inflammatory Activities of Thymoquinone against Microcystin-LR-Induced Hepatotoxicity and Neurotoxicity in Mice

“…In the biological system, oxidative stress comprises a sequence of events which involves the excessive production of ROS (O 2 •− (superoxide anions), OH • (hydroxyl radicals), H 2 O 2 (hydrogen peroxide), and NO (nitric oxide)) that overwhelms the cellular antioxidant defense mechanisms. These events cause several deleterious effects on cellular macromolecules such as lipid peroxidation, mitochondrial dysfunction, ATP reduction, protein oxidation, and DNA damage [38, 42, 43]. OH • is the most harmful ROS that directly attacks the lipid content of the cellular membranes causing lipid peroxidation manifested by increased production of MDA that also has the affinity to bind to other cell molecules which worsens the situation.…”