Lycopene abolishes palmitate-mediated myocardial inflammation in female Wistar rats via modulation of lipid metabolism, NF-κB signalling pathway, and augmenting the antioxidant systems.

BACKGROUND AND AIMS: Obesity-related heart failure is exacerbated by excessive intake of saturated fats such as palmitate (PA). Lycopene (LYC) possesses anti-lipidemic, antioxidant, cytoprotective, and anti-inflammatory effects. This study, therefore, evaluated the impact of LYC against PA-invoked cardiotoxicity. METHODS AND RESULTS: Thirty-six female rats were equally divided into six groups: control; PA (5 mM); PA + LYC (24 mg/kg); PA + LYC (48 mg/kg); LYC (24 mg/kg); and LYC (48 mg/kg). The PA was administered five times weekly for seven weeks, while the LYC was given for the last two weeks. Lipids in the blood and the heart were estimated, as were oxidative stress and antioxidant indices, cardiac function, inflammation, and histology. Palmitate overload occasioned a significant (p < 0.05) increase in cardiac cholesterol (50%), phospholipids (19%), and non-esterified fatty acids (40%). However, triglyceride levels decreased (38%). Furthermore, malondialdehyde (45%), hydrogen peroxide (33%) levels and myeloperoxidase activity increased (79%). Also, cardiac gamma-glutamyl transferase (50%), serum creatine kinase activities (1.34 folds), NF-kB, interleukin1ß, and interleukin-6 mRNA expression increased in the PA group relative to the control. In contrast, reduced glutathione (13%) and nitric oxide levels (22%), interleukin-10 mRNA expression, cardiac creatine kinase (35%), lactate dehydrogenase (33%), aspartate, and alanine transaminase activities decreased markedly (15- and 10%, respectively). Also, PA caused hyperemia, congestion of the cardiac interstitium, and infiltration of inflammatory cells. However, treatment with LYC reversed the features of cardiotoxicity and histological complications caused by PA. These observations are likely because LYC has anti-inflammatory, antioxidant, and cytoprotective properties. CONCLUSION: Thus, LYC might be an appropriate remedy to manage PA-induced cardiotoxicity in female rats.

Sub-acute exposure to Sudan IV-adulterated palm oil induces oxidative stress and represses the expression of Nrf2 and antioxidant genes in male albino rats.

This study investigated the effects of Sudan IV dye (S4D) on antioxidant biomarkers using palm oil adulterated with S4D. Thirty male albino rats were grouped into five (n = 6); Normal control, palm oil (PO), PO + S4D (100 mg/kg), PO + S4D (250 mg/kg), and S4D (250 mg/kg) for 21 days. Oxidative stress biomarkers were assessed in the serum, liver, and kidneys. Exposure to S4D (alone and in adulterated PO) occasioned significant depletions in the activities of SOD, CAT, and GPx, as well as GSH levels in the assessed compartments. Contrastingly, the levels of NO and MDA were significantly (p < 0.05) increased in the serum, liver, and kidney of rats exposed to PO + S4D (both doses) and S4D (250 mg/kg) when compared to control rats. Further, the expressions of the genes coding for CAT, GPx-1, GSR, and Nrf-2 were significantly (p < 0.05) down-regulated, relative to ß-actin, in groups exposed to S4D compared to the control. Interestingly, these parameters were not significantly different (p > 0.05) in the unadulterated PO-exposed rats compared to the control. These results show that S4D depleted the antioxidant capacities, while potentiating the generation of reactive species and oxidative damage. This study provides useful information on the oxidative mechanisms associated with consumption of S4D-containing consumer products.