3-iodo-l-tyrosine might play a role in Parkinson’s disease since this molecule is able, at high concentration, to inhibit tyrosine-hydroxylase activity, the rate-limiting enzyme in dopamine biosynthesis. The possible Parkinson-like effects of 3-iodo-l-tyrosine were tested on three experimental approaches in mice: cultured substantia nigra neurons, the enteric nervous system of the jejunum after intra-peritoneal infusions, and the nigrostriatal system following unilateral intrabrain injections. 3-iodo-l-tyrosine, a physiological molecule, was used at concentrations higher than its serum levels in humans. Parkinson-like signs were evaluated through abnormal aggregation of α-synuclein and tyrosine-hydroxylase, loss of tyrosine-hydroxylase-expressing and striatum-projecting neurons and fibers, reduced tyrosine-hydroxylase density, and Parkinson-like motor and non-motor deficits. The retrograde tracer FluoroGold was used in the brain model. The findings revealed that excess amounts of 3-iodo-l-tyrosine induce Parkinson-like effects in the three experimental approaches. Thus, culture neurons of substantia nigra show, after 3-iodo-l-tyrosine exposure, intracytoplasmic inclusions that express α-synuclein and tyrosine-hydroxylase. Intra-peritoneal infusions of 3-iodo-l-tyrosine cause, in the long-term, α-synuclein aggregation, thicker α-synuclein-positive fibers, and loss of tyrosine-hydroxylase-positive cells and fibers in intramural plexuses and ganglia of the jejunum. Infusion of 3-iodo-l-tyrosine into the left dorsal striata of mice damages the nigrostriatal system, as revealed through lower striatal tyrosine-hydroxylase density, reduced number of tyrosine-hydroxylase-expressing and striatum-projecting neurons in the left substantia nigra, as well as the emergence of Parkinson-like behavioral deficits such as akinesia, bradykinesia, motor disbalance, and locomotion directional bias. In conclusion, excess amounts of 3-iodo-l-tyrosine induce Parkinson-like features in cellular, enteric and brain approaches of Parkinsonism in mice.

3-碘-1-酪氨酸可能在帕金森氏病中起作用，因为该分子能够以高浓度抑制酪氨酸羟化酶活性，这是多巴胺生物合成中的限速酶。用三种实验方法在小鼠中测试了3-碘-1-酪氨酸可能产生的帕金森样效应：培养的黑质神经元，腹膜内注入后空肠的肠神经系统和单侧脑内注射后的黑质纹状体系统。3-碘升-酪氨酸是一种生理分子，其浓度高于人类血清中的浓度。通过α-突触核蛋白和酪氨酸羟化酶的异常聚集，酪氨酸羟化酶表达和纹状体投射神经元和纤维的丢失，酪氨酸羟化酶密度降低以及帕金森样运动和非运动缺陷来评估帕金森样体征。在脑模型中使用了逆行示踪剂FluoroGold。研究结果表明，在三种实验方法中，过量的3-碘-1-酪氨酸会诱发类似帕金森的效应。因此，黑质的培养神经元在暴露3-碘-1-酪氨酸后显示出表达α-突触核蛋白和酪氨酸羟化酶的胞浆内包涵体。3-碘的腹膜内输注升-酪氨酸长期导致α-突触核蛋白聚集，较厚的α-突触核蛋白阳性纤维，以及空肠壁内神经丛和神经节中酪氨酸羟化酶阳性细胞和纤维的丢失。3-碘的输注升-酪氨酸到小鼠损伤黑质纹状体系统的左背侧纹状体，如通过更低的纹状体酪氨酸羟化酶密度显示，减少的酪氨酸羟化酶表达和纹状体投射神经元的数目在左侧黑质，以及类似帕金森氏症的行为缺陷的出现，例如运动障碍，运动迟缓，运动失衡和运动方向偏向。总之，过量的3-碘-1-酪氨酸会在小鼠帕金森病的细胞，肠和脑途径中诱发帕金森样特征。