Carageorgiou Haris, Tzotzes Vassilios, Sideris Antonios, Zarros Apostolos, Tsakiris Stylianos
Department of Experimental Pharmacology, Medical School, University of Athens, Athens, Greece.
Basic Clin Pharmacol Toxicol. 2005 Nov;97(5):320-4. doi: 10.1111/j.1742-7843.2005.pto_174.x.
We have previously reported that cadmium (Cd) as 3CdSO4 . 8H2O decreases rat brain total antioxidant status and L-cysteine (Cys) has a protective effect against it. The aim of the present study was to investigate the effects of subacute Cd administration, either alone or (almost simultaneously) with zinc (Zn), calcium (Ca) and Cys, on brain acetylcholinesterase (AChE) activity and brain total antioxidant status in male adult rats. All substances were administered intraperitoneally. Cadmium (1 mg/kg/day for 14 days) increased AChE activity (+46%; P<0.001) and decreased total antioxidant status (-29%; P<0.001). Zinc and Ca (both 1 mg/kg/day for 14 days) increased AChE activity (+18%; P<0.01 and +53%; P<0.001) and caused no changes on rat brain total antioxidant status. L-Cysteine (7 mg/kg/day for 14 days) impressively increased AChE activity (+185%; P<0.001) and augmented total antioxidant status (+26%; P<0.001). In the groups of Zn+Cd, Ca+Cd and Cys+Cd co-administration, AChE activity remained high (+42%; P<0.001, +41%; P<0.001 and +141%; P<0.001 respectively), while total antioxidant status returned to the saline control levels. L-Cysteine given before a toxic dose of Cd (5 mg/kg) resulted in high AChE activity (+85%; P<0.001), a total antioxidant status similar to the control values, and survival of the treated rats. In conclusion, Cd increased brain AChE activity and decreased brain total antioxidant status of adult male rats. Zinc, Ca and Cys, given just before Cd administration, modified the Cd-induced effects and restored rat brain total antioxidant status to the control levels.
我们之前曾报道,作为3CdSO4·8H2O的镉(Cd)会降低大鼠大脑的总抗氧化状态,而L-半胱氨酸(Cys)对其具有保护作用。本研究的目的是调查亚急性给予镉,单独给予或(几乎同时)与锌(Zn)、钙(Ca)和L-半胱氨酸联合给予时,对成年雄性大鼠大脑乙酰胆碱酯酶(AChE)活性和大脑总抗氧化状态的影响。所有物质均通过腹腔注射给药。镉(1毫克/千克/天,共14天)使AChE活性增加(+46%;P<0.001),并降低总抗氧化状态(-29%;P<0.001)。锌和钙(均为1毫克/千克/天,共14天)使AChE活性增加(+18%;P<0.01和+53%;P<0.001),且对大鼠大脑总抗氧化状态无影响。L-半胱氨酸(7毫克/千克/天,共14天)显著增加AChE活性(+185%;P<0.001),并提高总抗氧化状态(+26%;P<0.001)。在锌+镉、钙+镉和半胱氨酸+镉联合给药组中,AChE活性仍然很高(分别为+42%;P<0.001、+41%;P<0.001和+141%;P<0.001),而总抗氧化状态恢复到生理盐水对照组水平。在给予毒性剂量的镉(5毫克/千克)之前给予L-半胱氨酸,导致AChE活性较高(+85%;P<0.001),总抗氧化状态与对照值相似,且经治疗的大鼠存活。总之,镉增加成年雄性大鼠大脑AChE活性并降低大脑总抗氧化状态。在镉给药前给予锌、钙和L-半胱氨酸,可改变镉诱导的效应,并将大鼠大脑总抗氧化状态恢复到对照水平。