The Mechanism of 2,4-Dichlorophenoxyacetic Acid Neurotoxicity on Rat Brain Tissue by Using FTIR Spectroscopy

Previous studies demonstrated that the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D), toxicity may be due to cell death by apoptosis. 2,4-D is approved to be associated with many disorders especially neurotoxicity. FTIR spectroscopy and transmission electron microscopy were used to investigate the neurotoxicity induced by LD50 dose of 2,4-D onto the cerebellum rat brain tissue. In response to 2,4-D stress, there is a significant increase in the intensities as well as bands area of 3463cm , 3276cm and 3165cm bands; the first band corresponds to the changes in the number of lipids hydroperoxyl and to lipid hydroxyl groups formed by oxidation. There are decrease in membrane lipid polarity, increase the disorder and the looseness of lipid chain packing and a significant increase in the formation of carbonyl compounds. Moreover, protein content and secondary structure were significantly influenced upon 2,4-D intoxication. Consistent with the IR results, EM analysis revealed morphological changes in the 2,4-D treated cerebellum tissue including nuclear damage with massive condensation of chromatin, mitochondrial matrix swelling, loss of cristae and rough endoplasmic reticulum dilatation and vesiculation. Thus, 2,4-D influences membrane lipid polarity, fluidity and protein order, in addition to the morphological changes all of which can be considered as apoptosis biomarkers. [Gehan A. Raouf, Safaa Y. Qusti, Awatef M. Ali. and Tahani H. Dakhakhni. The Mechanism of 2,4Dichlorophenoxyacetic Acid Neurotoxicity on Rat Brain Tissue by Using FTIR Spectroscopy Life Sci J 2012;9(4):1686-1697] (ISSN:1097-8135). http://www.lifesciencesite.com. 259