- 期刊
Investigation into the Mechanism by which 2,3,7,8-Tetrachlorodibenzo-p-dioxin Induces Dyschromatopsia by Measuring Electroretinogram Results and Cone Cell Quantification of Mice Exposed to TCDD
摘要
Purpose: TCDD is an environmental toxin that is exposed to humans in dangerous amounts most often through industrial accidents or occupational exposure. Studies of health effects of workers occupationally exposed to TCDD have connected the molecule to dyschromatopsia, but the mechanism of action by which dioxin induces color vision deficiency is unknown. This study sets out to experimentally examine whether TCDD is able to induce dyschromatopsia by damage to optic nerves or induce cell death in retinal cone cells directly. Methods: Damage to optic nerves will be measured by photopic electroretinogram tests on live mouse retinas and cone cell quantification will be performed by immunolabeling of mouse retina samples using goat anti-OPN1SW and rabbit anti-opsin red/green then viewing under fluorescent microscope. Possible results: Electroretinogram tests results may yield a (1) decrease in response levels indicating damage to optic nerves or (2) similar response levels indicating no damage to optic nerves. Cone cell quantification may lead to a (1) decrease in cone cell levels indicating apoptosis of retinal cells or (2) no change in cone cell levels indicating no direct effect on retinal cone cells. Conclusions: This study is able to determine if TCDD induces dyschromatopsia by one of two mechanisms (nervous system damage or cell apoptosis) but further investigations are needed to confirm the details of these mechanisms and examine mechanisms not investigated in this study.
參考文獻
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