Protective effects of protocatechuic acid on TCDD-induced oxidative and histopathological damage in the heart tissue of rats

Abstract

2,3,7,8-Tetracholorodibenzo-p-dioxin (TCDD) is a highly toxic environmental contaminant that causes severe toxic effects in animal and human. In this study, we investigated the toxic effects of TCDD and the preventive effects of protocatechuic acid (PCA), a widespread phenolic compound, in the heart tissue of rats. For this purpose, 3-4 months old 28 rats with 280-310 g body weights were equally divided into 4 groups (control, TCDD, PCA, TCDD + PCA group). A 2 μg/kg dose of 2,3,7,8-TCDD and 100 mg/kg dose of PCA were dissolved in corn oil and given orally to the rats for 45 days. The results indicated that TCDD induced oxidative stress by increasing the level of thiobarbituric acid reactive substance and by decreasing the levels of glutathione, catalase, glutathione peroxidase and superoxide dismutase in the heart tissue of rats. In contrast, PCA treatment prevents the toxic effects of TCDD on oxidative stress. In addition, histopathological alterations such as necrosis and hemorrhage occurred in TCDD group, and PCA treatment partially prevents these alterations in heart tissue. In this study, it was concluded that TCDD exposure led to toxic effects in heart tissue and PCA treatment could prevent the toxicity of TCDD.

Protective effects of melatonin against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cardiac injury in rats

“…It has been reported that oxidative stress from lipid peroxidation is mainly responsible for the cardiotoxicity produced by TCDD (Ciftci and Disli, 2013). In the present study, TCDD treatment led to a significant increase in the TBARS level, a decrease in the SOD, GSH and CAT levels in the heart when compared to the control group.…”

“…The ability of antioxidants to ameliorate toxic endpoints suggests that reactive oxygen species may mediate PHAH toxicity. Based on this relationship, Ciftci and Disli (2013) designed an experimental study to determine whether TCDD-induced heart damage is related to the reactive oxygen species production. In this study, protocatechuic acid was used as an antioxidant agent.…”

“…These contradicting results may be due in part to the differences of drug dose and exposure period, as well as the different sensitivity of systems used to detect MAP such as radio-telemetry, tail-cuff and invasive measurement by cannulation of carotid artery (the latter also being used in the current study). There appears to be a correlation between the acute TCDD exposure results in hypertension in days 2-3, the periodic normalizations of the blood pressure until day 23-29 and in the late phase, the hypotension that occurs in association with cardiomyopathy (Ciftci and Disli, 2013).…”

Amelioration of oxidative and inflammatory status in hearts of cholesterol-fed rats supplemented with oils or oil-products with extra virgin olive oil components

“…GSH is the most important non-enzymatic antioxidant compound that serves as an endogenous response to oxidative stress [3]. Heart GSH depletion has been linked to damage in heart tissue [45]. However, herein no tissue damage was reported in histological analysis (data not shown); therefore, GSH depletion was not detected.…”

A Review on Protocatechuic Acid and Its Pharmacological Potential

“…2,3,7,8-Tetrachlorodibenzo- p -dioxin (TCDD) [37] cardiotoxicity in 3-4 months old rats was studied and protocatechuic acid treatment at the dose of 100 mg/kg for 45 days was found to decrease the levels of TBARS, while increasing those of glutathione, catalase, glutathione peroxidase, and superoxide dismutase. Also PCA prevented histopathological alterations such as necrosis and hemorrhage in heart tissue induced by TCDD.…”