Objective. Manganese (Mn) has been reported, through dietary and occupational overexposure, to induce neurotoxicity named manganism. Pentoxifylline (PTX) administration attracts much attention considering the beneficial properties of PTX, as an anti-inflammatory and smooth muscle relaxation agent. This in vivo study aims to evaluate the effect of PTX on manganism in rat model. Materials and Methods. Thirty adult male Sprague Dawley rats received MnCl₂ (100 mg/kg, i.p. on days 1, 3, and 7) during a week alone or in combination with PTX (300 mg/kg, i.p. every day for 8 consecutive days on manganism rat model). Several locomotor activity indices, as well as biomarkers of oxidative stress, were monitored in the brain tissue of Mn-exposed animals. Results. It was found that PTX supplementation (300 mg/kg, i.p.) deteriorated the Mn-induced locomotor deficit. This drug also increased the Mn brain accumulation as well as reactive oxygen species (ROS) and lipid peroxidation products in the manganism rat model. Moreover, the levels of total antioxidant capacity (TAC) and glutathione (GSH) were shown to be reduced significantly compared to the control group. Conclusion. The results of this study revealed that PTX at a high dose (300 mg/kg) might increase manganism complications. PTX lowers the blood viscosity, improves the tissue perfusion, and increases the Mn levels in the brain.

中文翻译：

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己酮可可碱对锰中毒大鼠模型的影响：可能的毒性评估

目标。据报道，锰 (Mn) 通过饮食和职业过度接触会诱发称为锰中毒的神经毒性。考虑到 PTX 作为抗炎和平滑肌松弛剂的有益特性，己酮可可碱 (PTX) 给药引起了很多关注。这项体内研究旨在评估 PTX 对大鼠模型中锰中毒的影响。材料和方法。接收只成年雄性Sprague Dawley大鼠的MnCl ₂中单独一个星期或与PTX组合（300（100毫克/公斤，腹腔注射在第1天，第3，和7）毫克/公斤，腹膜内每天对锰中毒大鼠连续8天模型）。在暴露于锰的动物的脑组织中监测了几种运动活动指数以及氧化应激的生物标志物。结果。发现 PTX 补充剂 (300 mg/kg, ip) 恶化了 Mn 诱导的运动缺陷。该药物还增加了锰大鼠模型中的锰脑积累以及活性氧 (ROS) 和脂质过氧化产物。此外，与对照组相比，总抗氧化能力（TAC）和谷胱甘肽（GSH）的水平显着降低。结论。这项研究的结果表明，高剂量 (300 mg/kg) 的 PTX 可能会增加锰中毒的并发症。PTX 降低血液粘度，改善组织灌注，并增加大脑中的锰水平。