乙酰辅酶A羧化酶抑制剂的研究进展

乙酰辅酶A羧化酶(ACCase)是除草剂的作用靶标之一，此类除草剂主要有两类：芳氧苯氧丙酸类(APP)和环己烯酮类(环己二酮，环己烯二酮，CHD)。本文就ACCase抑制剂的发展历史、合成方法、结构与活性和除草机制等方面作了概述。     

Oxidative damage in bone and erythrocytes of suckling rats exposed to 2,4-dichlorophenoxyacetic acid

Nowadays, people’s exposure to pesticides such as 2,4-dichlorophenoxyacetic acid (2,4-D) is increasing continuously. This compound is suspected to produce in excess free radicals which have adverse effects on human health causing several cell alterations in the organism. The present study investigated oxidative stress in the bone and erythrocytes of suckling rats whose mothers were treated with 2,4-D. Experiments were carried out on adult Wistar rats given 600 mg/L of 2,4-D in their drinking water from the 14th day of pregnancy until day 14 after delivery. Exposing dams to 2,4-D caused disorders in the bone of their progeny. Indeed, it induced changes in bone mineralization, especially calcium and phosphorus levels. Moreover, total tartrate-resistant acid phosphatase, which reflected bone resorption, was enhanced while total alkaline phosphatase, which reflected bone formation, was reduced suggesting that this herbicide accelerated bone resorption. The impairment of bone function corresponded histologically.Rats exposed to 2,4-D showed in both bone and erythrocytes an increase in malondialdehyde, advanced oxidation protein products and protein carbonyl levels and a decrease in non-enzymatic (glutathione, non-protein thiol, and vitamin C) and enzymatic (superoxide dismutase, catalase, and glutathione peroxidase) antioxidant system.     

Selenium and vitamin E, natural antioxidants, protect rat cerebral cortex against dimethoate-induced neurotoxicity

Pesticides have been used in agriculture to enhance food production by eradicating unwanted insects and controlling disease vectors, nevertheless occupational exposure to high levels of these compounds can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study aims to determine the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress in cerebral cortex tissue induced by dimethoate, an organophosphorus pesticide. Adult Wistar rats were exposed either to dimethoate (0.2 g/L of drinking water), dimethoate + selenium (0.5 mg/kg of diet), dimethoate + vitamin E (100 mg/kg of diet), or dimethoate + selenium + vitamin E, for 30 days. Exposure to dimethoate increased malondialdehyde levels, protein carbonyl groups and advanced oxidation protein products, while Na⁺K⁺-ATPase, acetylcholinesterase and butyrylcholinesterase activities decreased in the cerebral cortex. An increase in glutathione peroxidase, superoxide dismutase and catalase activities and a decrease in glutathione, non-protein thiols and vitamin C levels were observed. Administration of selenium and/or vitamin E through the diet in dimethoate treated rats ameliorated the biochemical parameters cited above. The histological findings confirmed the biochemical results. The model of this study that we employed characterized the relationships between dimethoate-induced neurotoxicity and its alleviation by natural antioxidants like selenium and vitamin E. These elements may be considered beneficial for the protection of cerebral cortex against injury induced by dimethoate.