ABSTRACT
Objective
Acrylamide is a toxic compound widely used in industrial sectors. Acrylamide causes reactive oxygen species formation and the subsequent lipid peroxidation reaction, which plays an important role in the pathogenesis of oxidative damage. Taxifolin is a flavonoid with antioxidant properties that inhibit reactive oxygen species formation. In this study, we aimed to investigate the preventive effect of taxifolin on acrylamide-induced oxidative heart damage.
Methods
The rats were divided into three groups: Acrylamide, Acrylamide+Taxifolin , and Healthy group. Water and food intake and body weight alterations were recorded daily. Malondialdehyde, total glutathione, nuclear factor kappa-B, total oxidant status, and total antioxidant status levels were analyzed from the heart tissue. Troponin-I levels, the parameter known as a cardiac biomarker, were analyzed from the blood sample. The cardiac histopathologic examination was also performed.
Results
In the Acrylamide group animals, the malondialdehyde, nuclear factor kappa-B, total oxidant status, and troponin-I levels were significantly higher compared to the ones of Acrylamide+Taxifolin and Healthy groups. The levels of total glutathione and total antioxidant status were significantly lower compared to Acrylamide+Taxifolin and Healthy groups’. Additionally, in the Acrylamide group, body weight gain, food and water intake, significantly declined compared to the Acrylamide+Taxifolin and Healthy groups. However, in the Acrylamide+Taxifolin group, taxifolin supplementation brought these values close to Healthy group ones. Furthermore, taxifolin treatment ameliorated structural myocardial damage signs induced by acrylamide.
Conclusion
Acrylamide exposure significantly induced oxidative damage to rat heart tissue. Taxifolin was able to improve the toxic consequences of acrylamide biochemically and histopathologically, possibly due to its antioxidant properties.
Keywords
Acrylamide; Oxidative heart damage; Rat; Taxofilin
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Note: A: Bodyweight gain over two months in Acrylamide (ACL), Acrylamide+Taxifolin (TACL), and Healthy Group (HG) animals. In the ACL group animals, a significant decrease in body weight gain was recorded both by the end of the first month and at the end of the second month. B: Food intake over two months in ACL, TACL, and HG animals. In the ACL group animals, a significant decrease in food intake was recorded both by the end of the first month and at the end of the second month. C: Water intake over two months in ACL, TACL, and HG animals. In the ACL group animals, a significant water intake decrease was recorded both by the end of the first month and at the end of the second month.
Note: *p<0.001 according to ACL group. MDA: Malondialdehyde; tGSH: Total Glutathione; NF-ƘB: Nuclear Factor Kappa-B; TOS: Total Oxidant Status; and TAS: Total Antioxidant Status levels in the heart tissue and Troponin-I (TP-I) in the blood serum of study groups (n=6). Acrylamide (ACL) group compared to Healthy Group (HG) and Acrylamide+Taxifolin (TACL) groups.
Note: A: Substantial inflammatory cell infiltration (arrow) and vascular congestion (double arrow) in the heart tissue of the Acrylamide (ACL) group (H&E x 200). B: Hemorrhage and edema (arrow), myocardial degeneration, and loss of myofibrillar striation (double arrow) in the heart tissue of the ACL group (H&E 200). C: The decrease in the inflammatory cell infiltrate (arrow), vascular congestion (double arrow), and hemorrhage (zigzag arrow) were detected in the heart tissue of the Acrylamide+Taxifolin (TACL) group (H&E x 200).