Rosas-Jarquín Christian de Jesús, Rivadeneyra-Domínguez Eduardo, León-Chávez Bertha Alicia, Nadella Rasajna, Sánchez-García Aurora Del Carmen, Rembao-Bojórquez Daniel, Rodríguez-Landa Juan Francisco, Hernandez-Baltazar Daniel
Posgrado en Neuroetología, Instituto de Neuroetología, Universidad Veracruzana. Xalapa, Veracruz. Mexico.
Facultad de Química Farmacéutica Biológica, Universidad Veracruzana. Xalapa, Veracruz. Mexico.
Iran J Basic Med Sci. 2020 Jan;23(1):93-101. doi: 10.22038/IJBMS.2019.38460.9131.
Cassava ( Crantz) contains cyanogenic glycosides (linamarin and lotaustralin) that have been associated with neurological disorders in humans and rats. In basal ganglia, the dopaminergic neurons of substantia nigra (SNpc) show high cytotoxic susceptibility; therefore, the chronic consumption of cassava (CCC) could induce neurodegeneration in SNpc. In this study we examine the impact of CCC on the integrity of the nigrostriatal system, including apoptosis and microgliosis.
Male Wistar rats were administered cassava juice daily (3.57 g/kg and 28.56 g/kg, ) or linamarin (0.15 mg/ml, IP), and its effects were evaluated in rota-rod and swim tests at days 7, 14, 21, 28, and 35 of administration. In SNpc, oxidative/nitrosative stress was determined by malondialdehyde/4-hydroxyalkenals (MDA-4-HAD) and nitrite contents. Tyrosine hydroxylase immunoreactivity (TH-IR) was evaluated in SNpc, neostriatum (NE), and nucleus accumbens (NA). Apoptosis and microgliosis were determined by active-caspase-3 (C3) and CD11b/c (OX42) expression in the medial region of SNpc.
Chronic administration of cassava juice, or linamarin, increased motor impairment. The rats that received 28.56 g/kg cassava showed increased MDA-4-HAD content in SNpc and nitrite levels in NE with respect to controls. Significant loss of TH-IR in SNpc, NE, and NA was not found. The 28.56 g/kg cassava administration produced dopaminergic atrophy and microgliosis, whereas linamarin induced hypertrophy and C3-related apoptosis in SNpc.
CCC induces cellular stress on dopaminergic neurons, which could contribute to motor impairment in the rat.
木薯(Crantz)含有氰苷(亚麻苦苷和百脉根苷),这些氰苷与人类和大鼠的神经紊乱有关。在基底神经节中,黑质致密部(SNpc)的多巴胺能神经元表现出较高的细胞毒性易感性;因此,长期食用木薯(CCC)可能会诱导SNpc发生神经退行性变。在本研究中,我们研究了CCC对黑质纹状体系统完整性的影响,包括细胞凋亡和小胶质细胞增生。
每天给雄性Wistar大鼠灌胃木薯汁(3.57 g/kg和28.56 g/kg)或亚麻苦苷(0.15 mg/ml,腹腔注射),并在给药第7、14、21、28和35天通过转棒试验和游泳试验评估其效果。在SNpc中,通过丙二醛/4-羟基烯醛(MDA-4-HAD)和亚硝酸盐含量测定氧化/亚硝化应激。在SNpc、新纹状体(NE)和伏隔核(NA)中评估酪氨酸羟化酶免疫反应性(TH-IR)。通过SNpc内侧区域中活化的半胱天冬酶-3(C3)和CD11b/c(OX42)表达来确定细胞凋亡和小胶质细胞增生。
长期灌胃木薯汁或亚麻苦苷会增加运动功能障碍。与对照组相比,接受28.56 g/kg木薯的大鼠SNpc中的MDA-4-HAD含量增加,NE中的亚硝酸盐水平升高;未发现SNpc、NE和NA中TH-IR有显著损失。给予28.56 g/kg木薯导致多巴胺能萎缩和小胶质细胞增生,而亚麻苦苷诱导SNpc肥大和与C3相关的细胞凋亡。
CCC诱导多巴胺能神经元产生细胞应激,这可能导致大鼠出现运动功能障碍。