Haider Saida, Anis Lubna, Batool Zehra, Sajid Irfan, Naqvi Fizza, Khaliq Saima, Ahmed Shoaib
Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Karachi, 75270, Pakistan,
Metab Brain Dis. 2015 Feb;30(1):83-92. doi: 10.1007/s11011-014-9578-4. Epub 2014 Jul 1.
Cadmium is a toxic environmental and industrial pollutant. Cadmium toxicity has been reported to produce biochemical and behavioral dysfunction that may cause adverse effects on several organs including the central nervous system. The present study was designed to investigate the neurotoxic effects of Cadmium Chloride (CdCl2) at three different doses by using different behavioral models. Lipid peroxidation (LPO), superoxide dismutase (SOD) and acetylcholinesterase (AChE) activities were also monitored following acute intraperitoneal injection of cadmium. Twenty four adult locally bred Albino Wistar rats were divided into control and 3 test groups (n = 6). Control rats were injected intraperitoneally with saline (0.9% NaCl) and test groups were injected with CdCl2 (1 mg/kg, 2 mg/kg and 3 mg/kg) dissolved in physiological solution. Behavioral activities of rats were monitored after 1 h of cadmium injection. Locomotor activity and depression-like symptoms were measured by Open Field Test (OFT) and Forced Swimming Test (FST) respectively. Anxiety like behavior was monitored using Light-dark Transition (LDT) test and memory functions of rats were assessed by Morris Water Maze test (MWM). In the present study acute cadmium administration dose dependently increased anxiety in rats as compared to control rats. A significant increase in depression-like symptoms was also exhibited by cadmium treated rats. These behavioral dysfunctions may be attributed to the decreased superoxide dismutase (SOD) activity and simultaneously increased brain lipid peroxidation (LPO). Moreover learning and memory assessed by MWM showed dose dependent impairment in memory function in cadmium treated rats as compared to control rats. Acetylcholinesterase (AChE) activity was also decreased in brains of cadmium administered rats. It is suggested in this study that behavioral, biochemical and neurochemical dysfunctions caused by acute cadmium administration occur in a dose dependent manner.
镉是一种有毒的环境和工业污染物。据报道，镉毒性会导致生物化学和行为功能障碍，可能对包括中枢神经系统在内的多个器官产生不良影响。本研究旨在通过使用不同的行为模型，研究三种不同剂量的氯化镉（CdCl2）的神经毒性作用。在急性腹腔注射镉后，还监测了脂质过氧化（LPO）、超氧化物歧化酶（SOD）和乙酰胆碱酯酶（AChE）的活性。将24只成年本地饲养的白化Wistar大鼠分为对照组和3个试验组（n = 6）。对照组大鼠腹腔注射生理盐水（0.9% NaCl），试验组大鼠注射溶解在生理溶液中的CdCl2（1 mg/kg、2 mg/kg和3 mg/kg）。在注射镉1小时后监测大鼠的行为活动。分别通过旷场试验（OFT）和强迫游泳试验（FST）测量运动活动和抑郁样症状。使用明暗转换（LDT）试验监测焦虑样行为，并通过莫里斯水迷宫试验（MWM）评估大鼠的记忆功能。在本研究中，与对照组大鼠相比，急性镉给药剂量依赖性地增加了大鼠的焦虑。镉处理的大鼠也表现出抑郁样症状的显著增加。这些行为功能障碍可能归因于超氧化物歧化酶（SOD）活性降低，同时脑脂质过氧化（LPO）增加。此外，与对照组大鼠相比，通过MWM评估的学习和记忆显示镉处理的大鼠的记忆功能存在剂量依赖性损害。镉给药大鼠脑内的乙酰胆碱酯酶（AChE）活性也降低。本研究表明，急性镉给药引起的行为、生物化学和神经化学功能障碍以剂量依赖性方式发生。
