Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcellos 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil.
Biometals. 2012 Dec;25(6):1195-206. doi: 10.1007/s10534-012-9582-2. Epub 2012 Sep 19.
The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC. For this purpose, the rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 6-8): control/saline, NAC, Cd, and Cd/NAC. Cd exposure increased Cd concentration in plasma, spleen and thymus, and NAC co-treatment modulated this augment in both lymphoid organs. Cd exposure reduced red blood cell count, hemoglobin content and hematocrit value. Cd intoxication caused a decrease in total white blood cell count. NAC treatment per se caused an increase in lymphocyte and a decrease in neutrophil counts. On contrary, Cd exposure caused a decrease in lymphocyte and an increase in neutrophil and monocyte counts. NAC reversed or ameliorated the hematological impairments caused by Cd poisoning. There were no significant alterations in the NTPDase activity in lymphocytes of rats treated with Cd and/or NAC. Cd caused a decrease in the activities of lymphocyte AChE, whole blood AChE and serum BChE. However, NAC co-treatment was inefficient in counteracting the negative effect of Cd in the cholinesterase activities. The present investigation provides ex vivo evidence supporting the hypothesis that Cd induces immunotoxicity by interacting with the lymphoid organs, altering hematological parameters and inhibiting peripheral cholinesterase activity. Also, it highlights the possibility to use NAC as adjuvant against toxicological conditions.
本研究旨在通过评估暴露于 Cd 并联合 NAC 治疗的大鼠组织中的 Cd 浓度、血液学指标以及 NTPDase、乙酰胆碱酯酶 (AChE) 和丁酰胆碱酯酶 (BChE) 的活性，来研究 N-乙酰半胱氨酸 (NAC) 对 Cd 中毒的影响。为此，大鼠通过灌胃每天接受 Cd（2 mg/kg）和 NAC（150 mg/kg），每两天一次，共 30 天。动物分为四组（n = 6-8）：对照组/生理盐水、NAC、Cd 和 Cd/NAC。Cd 暴露增加了血浆、脾脏和胸腺中的 Cd 浓度，而 NAC 联合治疗调节了这两个淋巴器官中的这种增加。Cd 暴露降低了红细胞计数、血红蛋白含量和血细胞比容值。Cd 中毒导致总白细胞计数减少。NAC 治疗本身导致淋巴细胞计数增加，中性粒细胞计数减少。相反，Cd 暴露导致淋巴细胞计数减少，中性粒细胞和单核细胞计数增加。NAC 逆转或改善了 Cd 中毒引起的血液学损伤。用 Cd 和/或 NAC 处理的大鼠淋巴细胞中的 NTPDase 活性没有显著变化。Cd 导致淋巴细胞 AChE、全血 AChE 和血清 BChE 活性降低。然而，NAC 联合治疗在对抗 Cd 对胆碱酯酶活性的负面影响方面效率低下。本研究提供了离体证据，支持 Cd 通过与淋巴器官相互作用、改变血液学参数和抑制外周胆碱酯酶活性引起免疫毒性的假说。此外，它还突出了使用 NAC 作为对抗毒理学条件的辅助剂的可能性。
