Rotenone is widely used insecticide and pesticide. It is an environmental neurotoxin that induces accumulation of α-synuclein and deterioration of dopaminergic neurons in substantia nigra pars compacta (SNpc). Autophagymediated self-digestion of cytoplasmic inclusions may be defensive against neurodegeneration caused by rotenone toxicity. This study designed to assess the autophagy role in rotenone-induced neurotoxic effects. Sixteen C57 black 6 male mice were divided into rotenone & control groups, each group contains 8 mice: the rotenone group; mice were administrated rotenone (3 mg/kg/day intraperitoneally). In the control group carboxymethyl cellulose 0.5% (a vehicle for rotenone) was given as 3mL/Kg/day intraperitoneal. Neuro-behavioural locomotor tests, histopathological and immuno-histochemical analysis of the brain dopaminergic neuronal cells and counting of microtubule Associated Protein Light Chain 3 (LC3) positive cells expression were investigated. Results showed that rotenone administration increases the total distance travelled, numbers of line crossing, average speed, maximum speed and rotations of the animal's body. However, it significantly decreases the efficient path and the total mobile and immobile episodes and induced severe degenerative changes in histo-pathological examination. Also, it decreased significantly the quantity of LC3 positive cells in the brain sections of exposed mice i.e. neurodegeneration and inhibition of autophagy in dopaminergic system. From this study it can be concluded that rotenone can induce neurotoxicity through inhibition of autophagy.

Organophosphorus (OP) poisoning remains an important cause of morbidity and mortality in developing countries. Cardiac complications often accompany poisoning with these compounds, which are potentially preventable if they are recognized early and treated adequately. This study aimed to assess the potential benefit of plasma N-terminal pro brain natriuretic peptides (NT-proBNP) as an early marker of cardio toxicity induced by acute OP poisoning and to compare its beneficial value with the well-assessed cardiac markers serum "creatine kinase-MB (CK-MB) and cardiac Troponin I (cTnI)". This study was conducted on 150 individuals of both sexes. Participants were divided into three groups: Group I (control), group II (OP poisoning cases without cardiac signs) and group III (OP poisoning cases with cardiac signs). Serum levels of pseudocholinesterase (PCE), CK-MB, cTnI and plasma levels of NT-pro BNP were determined on admission. There were significant differences in plasma NT-proBNP levels between control group versus OP poisoned groups (II and III) and between groups II versus III with no significant differences regarding serum levels of CK-MB and cTnI. It can be concluded that plasma NT-proBNP can be used as an early marker and a diagnostic screening tool for silent myocardial stress that may occur early during the acute course of OP poisoning.

Previous studies showed that augmentation of the autophagy-lysosome process may be beneficial for many neurodegenerative diseases including Parkinson's disease (PD), in which abnormal accumulation of aggregated proteins and mitochondrial dysfunctions are considered as crucial pathogenesis. Recently, several studies have advocated the neuroprotective effects of intralipid in models of numerous neurodegenerative diseases. In this study, seventy "C57BL/6" mice divided into seven groups were used to evaluate the neuroprotective effects of autophagy enhancement using metformin and intralipid through neurobehavioural, a histopathological and immunohistochemical examination of rotenone-exposed mice brain. The mice were administrated rotenone (2.5 mg/kg intraperitoneally), metformin (100 mg/kg/day orally) and intralipid 20% (15 mL/kg intraperitoneal) daily for 4 weeks. Intralipid significantly recovered the damaged brain tissue and alleviated rotenone-induced brain damage. Furthermore, the co-administration of metformin and intralipid against rotenone produced more therapeutic efficiency. Intralipid exerted protection against rotenone-induced neuro-injuries to some extent through the autophagy process. The pharmacological induction of autophagy by intralipid may represent a novel therapeutic strategy as a disease-modifier in neurodegenerative diseases.

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