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首页> 外文期刊>Journal of applied toxicology >Tolerance to beta,beta'-iminodipropionitrile (IDPN)-induced neurobehavioural and vestibular toxicity in diabetic rats.
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Tolerance to beta,beta'-iminodipropionitrile (IDPN)-induced neurobehavioural and vestibular toxicity in diabetic rats.

机译：对β，β-酰上哌啶（IDPN）的耐受性 - 诱导糖尿病大鼠的神经侵蚀和前庭毒性。

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摘要

The present investigation was undertaken to study the neurotoxic effects of beta,beta'-iminodipropionitrile (IDPN) in normal, diabetic and insulin-treated diabetic rats. Sprague-Dawley male rats were divided into five groups: control, IDPN, diabetes, diabetes plus IDPN and diabetes plus insulin plus IDPN. The diabetes was induced with a single i.p. injection of streptozotocin (50 mg kg(-1)). One month after the induction of diabetes, the rats were treated with IDPN (100 mg kg(-1), i.p.) daily for 11 days. One of the diabetic groups treated with IDPN also received daily injection of insulin (25 U kg(-1), s.c.), 1 h before IDPN. The rats were observed daily for abnormal head movements and circling. The grip strength of the forelimbs was also measured. In the IDPN group the dyskinetic symptoms appeared on the 8th day, whereas the onset of dyskinesia was on the 12th day in IDPN-treated diabetic rats. The incidence and severity of dyskinesia were significantly higher in IDPN-treated normal (non-diabetic) rats as compared to IDPN-treated diabetic rats. The treatment of diabetic rats with insulin normalized striatal dopamine (DA) turnover but partially reversed diabetes-induced protection against IDPN dyskinesia. There was severe degeneration of sensory hair cells in crista ampullaris of IDPN-treated normal rats, whereas the diabetic rats showed significant protection against IDPN-induced vestibular hair cell degeneration. In conclusion, our study clearly demonstrates that diabetic rats are resistant to IDPN-induced neurobehavioural and vestibular toxicity. The results also show that diabetes-induced protection against IDPN-induced dyskinesia can be partially reversed by insulin. The mechanism behind the decreased vulnerability of diabetic animals to IDPN remains to be resolved. Further studies are warranted to investigate this paradoxical phenomenon.
机译：本研究旨在研究β，β-酰上哌啶（IDPN）在正常，糖尿病和胰岛素治疗的糖尿病大鼠中的神经毒性作用。 Sprague-Dawley雄性大鼠分为五组：对照，IDPN，糖尿病，糖尿病和IDPN和糖尿病加胰岛素加IDPN。用单一的I.P诱导糖尿病。注射链脲佐菌素（50mg kg（-1））。糖尿病诱导后一个月，每天用IDPN（100mg kg（-1），i.p.）处理大鼠11天。用IDPN处理的糖尿病族糖尿病组也接受了每日注射胰岛素（25μg（-1），S.C.），在IDPN之前1小时。每天观察大鼠用于异常头部运动和盘旋。还测量了前肢的抓握强度。在IDPN组中，第8天出现了动态症状，而障碍症的发作是在IDPN治疗的糖尿病大鼠中的第12天。与IDPN治疗的糖尿病大鼠相比，IDPN治疗的正常（非糖尿病）大鼠的发生率和严重程度显着高。用胰岛素归一化纹状体多巴胺（DA）转环的治疗糖尿病大鼠，但部分逆转糖尿病诱导对抗IDPN止吐作用的保护。在IDPN处理的正常大鼠的Crista Ampullaris中存在严重的感觉毛细胞变性，而糖尿病大鼠表现出对IDPN诱导的前庭毛细胞变性的显着保护。总之，我们的研究清楚地表明糖尿病大鼠对IDPN诱导的神经运动和前庭毒性有抗性。结果还表明，对IDPN诱导的止吐剂瘤的糖尿病诱导的保护可以部分地通过胰岛素反转。将糖尿病动物脆弱性降低的机制仍有待解决。有权进一步研究来调查这种矛盾的现象。

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