Oxidative Stress and Cardiovascular Diseases: The Role of Mitochondria

The redox status is determined by the balance between the production of reactive oxygen species (ROS) and their removal by the antioxidant defense system. Mitochondria, the center of oxidative metabolism and the principal site of ROS production, are crucial in health and also in the pathogenesis of many diseases. Mitochondrial dysfunction, resulting in a vicious cycle contributing to cellular damage and consequent cell death, has been proven to play a critical role in the pathogenesis of cardiovascular diseases. Previous studies have shown that mitochondrial transfer in cells plays a crucial role in regulating cardiovascular system development and maintaining normal tissue homeostasis. We review and evaluate in this chapter the evidence for mitochondrial dysfunction as a consequence of stress exposure and a contributing factor to cardiovascular diseases

Oxidative stress and histopathological changes induced by methylthiophanate, a systemic fungicide, in blood, liver and kidney of adult rats

Background: Methyl-thiophanate (MT), a fungicide largely used in agriculture throughout the world including Tunisia, protects many vegetables, fruits and field crops against a wide spectrum of fungal diseases. Oxidative stress has been proposed as a possible mechanism involved in MT toxicity on non-target organism.Methods: In the present study, the effect of MT injected intraperitoneally to adult rats at 300 or 500 mg/kg of body weight was studied on blood, liver and kidney.Results: Our results showed 3 days after MT injection, a significant decrease in hemoglobin and hematocrit values. A disruption in total white blood cells and platelets also occurred. Accordingly, an increased in malondialdehyde, H2O2 and advanced oxidation protein levels in liver and kidney were noted with the two doses. A significant change in plasma biomarkers and organ enzymatic and non-enzymatic activities were observed after MT treatment. The modifications in biochemical parameters were substantiated by histopathological data.Conclusion: These data confirmed the pro-oxidant effects of this fungicide. Accordingly, care must be taken to avoid mammalian and human exposure to MT.Keywords: Methyl-thiophanate, white blood cells, red blood cells, liver, kidne

Oxidative stress and histopathological changes induced by methylthiophanate, a systemic fungicide, in blood, liver and kidney of adult rats.

Background: Methyl-thiophanate (MT), a fungicide largely used in agriculture throughout the world including Tunisia, protects many vegetables, fruits and field crops against a wide spectrum of fungal diseases. Oxidative stress has been proposed as a possible mechanism involved in MT toxicity on non-target organism. Methods: In the present study, the effect of MT injected intraperitoneally to adult rats at 300 or 500 mg/kg of body weight was studied on blood, liver and kidney. Results: Our results showed 3 days after MT injection, a significant decrease in hemoglobin and hematocrit values. A disruption in total white blood cells and platelets also occurred. Accordingly, an increased in malondialdehyde, H2O2 and advanced oxidation protein levels in liver and kidney were noted with the two doses. A significant change in plasma biomarkers and organ enzymatic and non-enzymatic activities were observed after MT treatment. The modifications in biochemical parameters were substantiated by histopathological data. Conclusion: These data confirmed the pro-oxidant effects of this fungicide. Accordingly, care must be taken to avoid mammalian and human exposure to MT

Protective effect of selenium against aluminium chloride induced cardiotoxicity in rats

Our study pertains to evaluate the protective effect of selenium (Se), used as a nutritional supplement, against aluminium chloride induced cardiotoxicity in rats. Rats have received during 21 days either AlCl3 (400 ppm) via drinking water, AlCl3 associated with Na2SeO3 (0.5 mg/kg of diet) or only Na2SeO3. Co-administration of Se to AlCl3 treated rats alleviated heart oxidative stress objectified by a decrease of malondialdehyde, hydrogen peroxide and protein carbonyls levels. An improvement in antioxidant redox status, enzymatic (catalase, superoxide dismutase and glutathione peroxidase) and non enzymatic (reduced glutathione, non protein thiols and vitamin C) was also observed in Se treated rats.  LDH and CK activities, TC, LDL-C levels, TC/HDL-C and LDL-C/HDL-C ratios were increased, while HDL-C and TG decreased in rats treated with AlCl3. Cardiac biomarkers and lipid profile were restored to near control values by the supplementation of Se. Our results revealed that Se, a trace element with antioxidant properties, was effective in preventing heart damage induced by aluminium chloride

Citrus aurantium L. peel extract mitigates hexavalent chromium-induced oxidative stress and cardiotoxicity in adult rats

In the present study, we aimed to examine the potential protective effect of C. aurantinum L. peel extract against oxidative damage induced by hexavalent chromium in the heart of adult rats. Rats were divided into six groups. Group I served as controls and received standard diet. Group II received via drinking water potassium dichromate (K2Cr2O7) alone (700 ppm) during 3 weeks. Groups III and IV were pre-treated for 10 days by gavage with the ethanolic extract of C. aurantium peels at doses of 100 and 300 mg/kg body weight/day, respectively, and then K2Cr2O7 was administrated during 3 weeks. Groups V and VI received by gavage only C. aurantium peel ethanolic extract at doses of 100 and 300 mg/kg body weight/day, respectively, during 10 days. K2Cr2O7 treatment increased the cardiac levels of malondialdehyde (MDA), protein carbonyls (PCO), advanced oxidation protein products (AOPP), non-protein thiols, glutathione and vitamin C, as well as the activities of catalase, superoxide dismutase and glutathione peroxidase. Cardiac histological alterations, manifested by hemorrhage and cytoplasmic vacuolization, were also observed. Pre-treatment with C. aurantium peel extract (300 mg/kg) attenuated significantly the biochemical and histopathological changes observed following K2Cr2O7 exposure in rat’s heart. Our findings indicated that C. aurantium peel extract was able to hamper K2Cr2O7-induced myocardial injury, which could be attributed to its antioxidant activity

Extra Virgin olive oil mitigates hematotoxicity induced by acrylamide and oxidative damage in adult rats

Acrylamide (ACR) is a dietary contaminant derived from a wide range of foods through the Maillard-reaction during the cooking process. The present study focused on the hematotoxic effects of ACR and the protective efficacy of Extra Virgin olive oil (EVOO) in alleviating hematotoxicity and oxidative stress in erythrocytes of adult rats. Rats were divided into four groups of six each: group 1, serving as negative controls, received distilled water; group 2 received by  gavage ACR at a dose of 40 mg/ kg body weight; group 3 received by gavage ACR supplemented with EVOO (300 μL); group 4,serving as positive controls, received only EVOO by gavage. All groups were sacrificed after three weeks. Acrylamide induced a significant increase in white blood cells (WBC), erythrocyte osmotic fragility (OF) and a decrease in red blood cells (RBC), hemoglobin (Hb) and hematocrit (Ht). While mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) remained unchanged. Furthermore, exposure of rats to ACR induced erythrocytes oxidative stress with an increase of malondialdehyde, hydrogen peroxide, and protein carbonyls levels. A reduction in antioxidant status, enzymatic (catalase, glutathione peroxidase and superoxide dismutase) and non enzymatic (reduced glutathione, non protein thiols and vitamin C) was observed when compared to controls. EVOO supplementation alleviated significantly hematotoxicity induced by acrylamide as evidenced by restoring the biochemical markers cited above to near normal values. Our results revealed that extra virgin olive oil, a main component of olive Mediterranean diet, was effective in preventing erythrocytes damage and oxidative stress

Nitraria retusa fruit prevents penconazole-induced kidney injury in adult rats through modulation of oxidative stress and histopathological changes

Context: Nitraria retusa (Forssk.) Asch. (Nitrariaceae) is a medicinal plant which produces edible fruits whose antioxidant activity has been demonstrated. Objective: The current study elucidates the potential protective effect of N. retusa fruit aqueous extract against nephrotoxicity induced by penconazole, a triazole fungicide, in the kidney of adult rats. Materials and methods: Adult Wistar rats were exposed either to penconazole (67 mg/kg body weight), or to N. retusa extract (300 mg/kg body weight) or to their combination. Penconazole was administered by intra-peritoneal injection every 2 days from day 7 until day 15, the sacrifice day, while N. retusa extract was administered daily by gavage during 15 days. Oxidative stress parameters, kidney biomarkers and histopathological examination were determined. Results: Nitraria retusa extract administration to penconazole treated rats decreased kidney levels of malondialdehyde (−10%), hydrogen peroxide (−12%), protein carbonyls (PCOs, −11%) and advanced oxidation protein products (AOPP, −16%); antioxidant enzyme activities: catalase (−13%), superoxide dismutase (−8%) and glutathione peroxidase (GPx, −14%), and the levels of non-enzymatic antioxidants: non-protein thiols (−9%), glutathione (−7%) and metallothionein (−12%). Furthermore, this plant extract prevented kidney biomarker changes by reducing plasma levels of creatinine, urea, uric acid and LDH and increasing those of ALP and GGT. Histopathological alterations induced by penconazole (glomeruli fragmentation, Bowman’s space enlargement, tubular epithelial cells necrosis and infiltration of inflammatory leucocytes) were attenuated following N. retusa administration. Discussion and conclusion: Our results indicated that N. retusa fruit extract had protective effects against penconazole-induced kidney injury, which could be attributed to its phenolic compounds