No abstract

No abstract

No abstract

No abstract

No abstract

The extensive use of Lambda-cyhalothrin (LCT) has been associated with the various toxicities that non-target organisms can undergo including mammals. However, the mechanism of induced-LCT cytotoxicity in animal brain cells is still elusive, particularly in brain regions, notably the hippocampus, an area directly involved in cognitive function. This study aimed to investigate the neurotoxic effects in the rat hippocampus chronically exposed to LCT (0.18 mg/kg and 0.36 mg/kg), and the neuroprotective potential of Melissa officinalis L methanol extract (MOE) (200 mg/kg) against this toxicity. After experimental period (90 days), the redox status, the functional and structural integrity of the hippocampus mitochondria as well as the apoptotic signaling pathway were evaluated. The current findings suggest that LCT produces imbalance of mitochondrial redox status expressed by, on one side, increasing of stress markers such as protein carbonyls (PCO), malondialdehyde (MDA), and hydrogen peroxide (H2O2) levels; and on the other side, by a decline in the potential of antioxidant systems, namely the level of mitochondrial enzymatic activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH).This study also showed an increase in mitochondrial permeability, along with mitochondrial edema and considerable decrease in its O2 consumption. Moreover, the same results recorded an increase in caspase-3 and cytosolic cytochrome-c. Conversely, this study proved that all these toxic aspects induced by LCT were significantly mitigated when the administration of this synthetic pyrethroid was associated with MOE. Taken together, data of this study shed light on mitochondrial damage and apoptosis stimulation under the toxic effect of LCT and suggests that MOE is endowed with potent neuroprotective effect, possibly via its antioxidant and antiapoptotic properties.

During recent years the defensive role of diferuloylmethane against oxidative stress and apoptosis has been experimentally documented. Fe3O4-NPs can cause cellular death by inducing oxidative stress. Present study aimed to investigate whether diferuloylmethane could protect rats mitochondria against Fe3O4-NPs intoxication. Twenty adult male rats were randomly chosen and divided into four groups: control; treated with 10 mg/kg/d of Fe3O4-NPs; treated with diferuloylmethane at the dose 20 ml/kg/d; treated with Fe3O4-NPs (10 mg/kg/d) and diferuloylmethane (20 ml/kg/d) respectively for 28 days. The results showed that Fe3O4-NPs increased the Alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid peroxidation, mit-GSH (Glutathione), mit-CAT (Catalase), mit-GST (Glutathione S-transferase) and decreased mit-GPx (Glutathione peroxidase), with increased in mitochondrial swelling and permeability followed by the increasing level of plasmatic Cyt-c. The addition of diferuloylmethane (DFM) to these samples reduces or corrects the amount of the most of biomarkers. These findings have demonstrated that DFM can act as an antioxidant and antiapoptotic factor against damages induced by Fe3O4-NPs.

The enhanced uses of nanoparticles in our daily life have been augmented according to industrial development. Indeed, the nature and the properties of nanoparticles make them a good choice in many products from food enhancers, drugs, nanomaterials, medicine, electronics and cosmetics.Our study is a trial on the effects of AlNPs (<10nm) on the mitochondrial status and possible dysfunction in detoxication organ of the snail Helix sp. and to assess the impact of these nanomaterials on swelling, permeability and respiration of hepatopancreatic mitochondria.Obtained results presents an increased activity of many mitochondrial metabolization enzymes (mitGST, mitCAT, mitMDA, mitGPx) and a decrease in GSH level. Thus, an increase in mitochondrial swelling and permeability have been showed with a slow rate of respiration level according to the controls group.Finally, our results suggested that nanoparticles of aluminum affect directly the mitochondrial function by the perturbation of general metabolic status of snails exposed to 5 and 10μg /g of NPs of Al each 2 days.