Chowdhury M Jasim, Wood Chris M
Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario, Canada L8S 4K1.
Comp Biochem Physiol C Toxicol Pharmacol. 2007 Apr;145(3):321-32. doi: 10.1016/j.cbpc.2007.01.004. Epub 2007 Jan 26.
Renal function was examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 52 d and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Dietary Cd had no major effects on UFR (urine flow rate) and GFR (glomerular filtration rate) but caused increased renal excretion of glucose, protein, and major ions (Mg(2+), Zn(2+), K(+), Na(+), Cl(-) but Ca(2+)). However, dietary Cd did not affect any plasma ions except Na(+) which was significantly elevated in the Cd-acclimated trout. Plasma glucose and ammonia levels fell by 25% and 36% respectively, but neither plasma nor urine urea was affected in Cd-acclimated fish. Dietary Cd exposure resulted in a remarkable increase of Cd load in the plasma (48-fold, approximately 22 ng/mL) and urine (60-fold, 8.9 ng/mL), but Cd excretion via the kidney was negligible on a mass-balance basis. Clearance ratio analysis indicates that all ions, Cd, and metabolites were reabsorbed strongly (58-100%) in both naïve and dietary Cd exposed fish, except ammonia which was secreted in both groups. Mg(2+), Na(+), Cl(-) and K(+) reabsorption decreased significantly (3-15%) in the Cd-exposed fish relative to the control. Following waterborne Cd challenge, GFR and UFR were affected transiently, and only Mg(2+) and protein excretion remained elevated with no recovery with time in Cd-acclimated trout. Urinary Ca(2+) and Zn(2+) excretion rates dropped with an indication of renal compensation towards plasma declines of both ions. Cadmium challenge did not cause any notable effects on urinary excretion rates of metabolites. However, a significant decrease in Mg(2+) reabsorption but an increase in total ammonia secretion was observed in the Cd-acclimated fish. The study suggests that dietary Cd acclimation involves physiological costs in terms of renal dysfunction and elevated urinary losses.
对成年虹鳟(Oncorhynchus mykiss)进行研究,使其长期暴露于亚致死水平的膳食镉(500毫克/千克饲料)中52天,随后在接下来的72小时内对其进行水体镉(10微克/升)刺激。膳食镉对尿流率(UFR)和肾小球滤过率(GFR)没有重大影响,但导致肾脏对葡萄糖、蛋白质和主要离子(Mg(2+)、Zn(2+)、K(+)、Na(+)、Cl(-),但Ca(2+)除外)的排泄增加。然而,膳食镉除了使镉适应组的虹鳟体内的Na(+)显著升高外,对任何血浆离子均无影响。血浆葡萄糖和氨水平分别下降了25%和36%,但镉适应组的鱼的血浆和尿液尿素均未受影响。膳食镉暴露导致血浆(48倍,约22纳克/毫升)和尿液(60倍,8.9纳克/毫升)中的镉负荷显著增加,但从质量平衡的角度来看,通过肾脏排出的镉可以忽略不计。清除率分析表明,在未接触镉和膳食镉暴露的鱼中,除了两组都分泌的氨外,所有离子、镉和代谢物都被大量重吸收(58 - 100%)。相对于对照组,镉暴露组的鱼对Mg(2+)、Na(+)、Cl(-)和K(+)的重吸收显著降低(3 - 15%)。在水体镉刺激后,GFR和UFR受到短暂影响,在镉适应组的虹鳟中,只有Mg(2+)和蛋白质排泄仍然升高,且未随时间恢复。尿Ca(2+)和Zn(2+)排泄率下降,表明肾脏对这两种离子的血浆含量下降进行了代偿。镉刺激对代谢物的尿排泄率没有造成任何显著影响。然而,在镉适应组的鱼中,观察到Mg(2+)重吸收显著降低,但总氨分泌增加。该研究表明,膳食镉适应在肾功能障碍和尿流失增加方面涉及生理代价。