Manganese Induces Oxidative Stress, Redox State Unbalance and Disrupts Membrane Bound ATPases on Murine Neuroblastoma Cells In Vitro: Protective Role of Silymarin

Manganese (Mn) is an essential trace element required for ubiquitous enzymatic reactions. Chronic overexposure to this metal may promote potent neurotoxic effects. The mechanism of Mn toxicity is not well established, but several studies indicate that oxidative stress play major roles in the Mn-induced neurodegenerative processes. Silymarin (SIL) has antioxidant properties and stabilizes intracellular antioxidant defense systems. The aim of this study was to evaluate the toxic effects of MnCl2 on the mouse neuroblastoma cell lines (Neuro-2A), to characterize the toxic mechanism associated with Mn exposure and to investigate whether SIL could efficiently protect against neurotoxicity induced by Mn. A significant increase in LDH release activity was observed in Neuro-2A cells associated with a significant decrease in cellular viability upon 24 h exposure to MnCl2 at concentrations of 200 and 800 μM (P < 0.05) when compared with control unexposed cells. In addition, exposure cells to MnCl2 (200 and 800 μM), increases oxidant biomarkers and alters enzymatic and non enzymatic antioxidant systems. SIL treatment significantly reduced the levels of LDH, nitric oxide, reactive oxygen species and the oxidants/antioxidants balance in Neuro-2A cells as compared to Mn-exposed cells. These results suggested that silymarin is a powerful antioxidant through a mechanism related to its antioxidant activity, able to interfere with radical-mediated cell death. SIL may be useful in diseases known to be aggravated by reactive oxygen species and in the development of novel treatments for neurodegenerative disorders such as Alzheimer or Parkinson 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

Beneficial Effects of Extra Virgin Olive Oil Rich in Phenolic Compounds on Cardiovascular Health

The Mediterranean diet (Med-diet) includes a high consumption of cereals, fruits, legumes and vegetables, a moderate fish intake and a low consumption of red meat. Olive oil is a basic component of the Med-diet due to its numerous health benefits. In the last decade, many epidemiological studies have confirmed the protective role of extra virgin olive oil (EVOO) against several chronic illnesses including cardiovascular diseases. EVOO is mainly composed of triacylglycerols, with oleic acid as the dominating esterified fatty acid, and other minor compounds. Among them, phenolic compounds, such as hydroxytyrosol and its derivatives (oleuropein and tyrosol), are the principal components responsible for the cardioprotective effects. They are endowed with wide biological activities, including strong antioxidant properties, allowing the prevention of cardiovascular risk factors, such as atherosclerosis, plasma lipid disorders, endothelial dysfunction, hypertension, obesity and type 2 diabetes. The aim of the present chapter was to elucidate the beneficial effect of EVOO, as part of the Mediterranean-style diets, on cardiovascular risk factors and to discuss the underlying mechanisms by which polyphenols exert their effects

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

Effect of selenium on hypothyroidism induced by methimazole (MMI) in lactating rats and their pups

The present study was undertaken to assess the effect of selenium (Se) on hypothyroidism induced by methimazole (MMI) in lactating rats and their pups. Rats were randomly divided into four groups of six each: group I served as a negative control which received standard diet; group II received orally MMI (250 mg L–1); group III received both MMI (250 mg L–1, orally) and Se (0.5 mg/kg of diet); group IV served as a positive control and received Se (0.5 mg Na2 SeO3 /kg of diet). Treatments were started from the 14th day of pregnancy until postnatal day 14. In the MMI-exposed group, the body weight of 14-dayold pups diminished compared to controls; besides, a hypertrophy of the thyroid glands was observed. Co-administration of Se through the diet restored these parameters to near normal values. In the MMItreated group, thyroid iodine contents and plasma thyroid hormone levels significantly decreased, while plasma TSH levels increased in pups and their mothers. These biochemical modifications corresponded histologically to closed follicles, increased vascularity and a reduction in colloid volume. Co-treatment with Se ameliorated these parameters. We concluded that the supplementation of Se in diet had beneficial effects on hypothyroidism during a critical period of life

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.&nbsp; 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