镉胁迫下NO对胡杨细胞Cd2+吸收调控机制的研究

本文研究了NO对胡杨愈伤细胞Cd2+耐受性的影响。结果表明:Cd2+(50 μmol/L)显著抑制了胡杨细胞的生长,而硝普钠SNP(NO供体,25 μmol/L)能明显缓解Cd2+对胡杨细胞生长的抑制作用,并减轻镉对细胞膜的伤害以及镉胁迫导致的细胞活力下降。利用非损伤微测技术等研究了NO对Cd2+动态吸收的影响。CdCl2(50 μmol/L)处理之后,胡杨细胞表现出Cd2+内流,而SNP(25 μmol/L,6 h)显著抑制了Cd2+的内流,并降低了Cd2+在细胞内的积累。研究发现,NO是通过调控钙离子通道来抑制胡杨细胞对Cd2+的吸收。镉胁迫下Cd2+内流被钙离子通道专一性抑制剂氯化镧明显抑制,表明Cd2+是通过钙离子通道转运进入细胞。并且发现,NO是通过促进Ca2+的内流来竞争性地抑制胡杨细胞对Cd2+的吸收,从而缓解了镉胁迫对胡杨细胞造成的生长抑制。 

Mediation of NO on Cd2+ uptake in Populus euphratica cells under cadmium stress

We investigated the effect of nitric oxide (NO)on cadmium (Cd2+) tolerance in Populus euphratica cells.Results showed that 50 μmol/L Cd2+ significantly restricted cell growth; however, the inhibition of Cd2+ on cell growth was evidently alleviated by the addition of sodium nitroprusside (SNP, nitric oxide donor, 25 μmol/L). Moreover, SNP could relieve the decline of Cd2+-induced cell viability and damage to membrane during the period of cadmium stress. The effect of NO on cadmium kinetics was investigated using the non-invasive micro-test technique (NMT). After being subjected to 50 μmol/L CdCl2solution, P. euphratica showed a substantial Cd2+ influx. However, the cadmium-induced Cd2+ influx and the subsequent accumulation were both significantly restricted by 25 μmol/L SNP. Furthermore, pharmacological experiments showed that NO mediated the Cd2+ entry through calcium permeable channels in P.euphratica. The Cd2+ influx caused by Cd2+ stress was strongly inhibited by lanthanum chloride, a specific inhibitor of calcium channels. Noteworthy, NO was found to increase Ca2+ influx, which competitively inhibited the entry of Cd2+ through calcium permeable channels.Consequently, the Cd2+ uptake and buildup were limited, and thus the growth inhibition by cadmium was alleviated in P. euphratica cells.