Abstract：
Litchi (Litchi sinensis), a fruit with a sweet and white aril, cultivated mainly in Southeast Asia and possesses anticancer, antibacterial, antioxidant, and other therapeutic properties. It is a delicacy among children. However, an outbreak of acute encephalopathy syndrome (AES) in litchi growing regions during the seasons of litchi ripening and harvesting (May-June) resulted in symptoms of lethargy, weakness, fever, vomiting, seizures, and coma that was most common among malnourished children below 15 years. Upon successful epidemiological studies, it was confirmed that the non-protein amino acids such as hypoglycine A (HGA) and methylenecyclopropylglycine (MCPG) are responsible for the AES outbreak. Most of the underprivileged and malnourished kids with an empty stomach venture into the litchi orchards to savor the fruit during the litchi harvesting season. Their fasting condition results in decreased glucose levels in the blood. The decreased glucose levels trigger glycogenolysis. However, gluconeogenesis takes over glycogenolysis to replenish the glucose levels due to fewer glycogen stores in malnourished children. The toxins are involved in fatty acid oxidation and gluconeogenesis pathways, by blocking several steps in the former process. Depleted glycogen stores and suppression of gluconeogenesis synergistically cause hypoglycemia and accumulation of toxic intermediates from the metabolic pathway leading to metabolic failure. The incidence of AES can be prevented by creating proper awareness among the farmers, vendors and consumers on the importance of adverse effects of litchi fruit when consumed on empty stomach or fasting state. Further, elucidating detailed biochemical pathway of HGA and MCPG toxicity, improving agricultural and public health practices, keeping glucose stores and glucose banks in the areas which are highly prone to litchi induced toxicity are some of the therapeutic measures. This review highlights and discusses the AES incidences, mechanistic pathways involved in litchi fruit toxicity, and corresponding risk factors involved and possible treatment and preventive approaches.
摘要：
荔枝(Litchisinensis),一种带有甜美白色假种皮的水果，主要在东南亚种植，具有抗癌作用，抗菌，抗氧化剂，和其他治疗特性。这是孩子们的美味。然而,在荔枝成熟和收获的季节（5月至6月），荔枝生长地区爆发了急性脑病综合征（AES），导致嗜睡症状，弱点,发烧,呕吐,癫痫发作,以及在15岁以下营养不良儿童中最常见的昏迷。根据成功的流行病学研究，已证实,非蛋白质氨基酸如低甘氨酸A(HGA)和亚甲基环丙基甘氨酸(MCPG)是AES爆发的原因.大多数贫困和营养不良的孩子空着肚子冒险进入荔枝园，在荔枝收获季节品尝水果。他们的禁食状况导致血液中的葡萄糖水平降低。降低的葡萄糖水平引发糖原分解。然而,由于营养不良儿童的糖原储存较少，糖异生接管糖原分解以补充葡萄糖水平。这些毒素参与脂肪酸氧化和糖异生途径，通过阻止前一个过程中的几个步骤。消耗的糖原储存和糖异生的抑制协同地引起低血糖和来自代谢途径的毒性中间体的积累,导致代谢失败。通过在农民中建立适当的意识，可以防止AES的发生，供应商和消费者对荔枝果实在空腹或禁食状态下食用时的不利影响的重要性。Further,阐明HGA和MCPG毒性的详细生化途径，改善农业和公共卫生实践，在容易发生荔枝毒性的地区保持葡萄糖储备和葡萄糖库是一些治疗措施。这篇评论强调并讨论了AES的发生率，荔枝果实毒性的机制途径，以及所涉及的相应危险因素以及可能的治疗和预防方法。
