碳酸盐碱度对青海湖裸鲤幼鱼肝和肾SOD、ACP和AKP酶活性的影响

Effects of carbonate alkalinity stress on SOD,ACP,and AKP activities in the liver and kidney of juvenile Gymnocypris przewalskii

青海湖裸鲤(Gymnocypris przewalskii,以下简称裸鲤)为耐盐碱鱼类。自青海湖裸鲤救护中心取裸鲤幼鱼,全长(4.42±0.02)cm,体质量(0.84±0.01)g。碳酸盐碱度暴露浓度设定为32 mmol/L(CA32)和64 mmol/L(CA64),通过测定青海湖裸鲤幼鱼肝和肾中超氧化物歧化酶(SOD)、酸性磷酸酶(ACP)和碱性磷酸酶(AKP)酶活性变化规律,探索裸鲤幼鱼肝和肾中SOD、ACP和AKP对碳酸盐碱度胁迫的生理响应。在本试验范围内,裸鲤在高碱环境中显示出较强的适应调节能力,在碳酸盐碱度胁迫下,SOD、ACP和AKP酶活性均能在发生显著变化后快速恢复到初始水平,但3种酶显示出不同的变化规律:(1)肝SOD在CA32和CA64胁迫3 d、肾SOD在CA32胁迫4 d、CA64胁迫3 d时,酶活性均显著升高。(2)肝和肾ACP活性出现不同的变化趋势,肝ACP活性仅在CA64胁迫组4 d出现显著上升,而肾ACP活性在CA32胁迫0.5 d、7 d和CA64胁迫1 d时分别出现了显著性波动。(3)肝AKP在CA32胁迫1 d、CA64胁迫3 d时,酶活性显著升高,而肾AKP仅在CA32胁迫0.5 d时,酶活性显著升高。在碳酸盐碱度胁迫下,3种酶活性均能发生显著变化,说明青海湖裸鲤幼鱼通过抗氧化及去磷酸化应激调节,来更好地应对高碱环境。

Saline-alkaline water is relatively prevalent throughout China. High alkalinity is thought to represent a significant stressor for aquatic organisms that occupy saline-alkaline waters. Gymnocypris przewalskii is a com- mercially important fish that is endemic to Qinghai Lake, a high saline-alkali environment. This species is ana- dromous and migrates up rivers to spawn between April to July. The abundance of G. przewalskii has decreased dramatically because of over-fishing and habitat degradation. As a result, it is now listed as an endangered fish. Thus, an understanding of the changes in stress-related enzymes in the liver and kidney of juvenile G. przewalskii exposed to carbonate alkalinity （CA） may prove useful for protecting the remaining G. przewalskii resource. We exposed juvenile G. przewalskii to 32 or 64 mmol/L carbonate alkalinity stress and measured the activity of su- peroxide dismutase （SOD）, acid phosphatase （ACP）, and alkaline phosphatase （AKP） in the liver and kidney 0.25, 0.5, 1, 2, 3, 4, 5, 7, and 9 d after the initial exposure. SOD is involved in the elimination of reactive oxygen species, which are produced following exposure to environmental stressors, whereas ACP and AKP assist in the elimination of metabolic products by dephosphorylation. The activity of both liver and kidney SOD initially increased with exposure time then returned to control levels. Liver SOD activity peaked in the CA32 and CA64 groups on day 3, whereas kidney SOD activity peaked on days 4 and 3, respectively. Interestingly, carbonate alkalinity stress pro- moted ACP activity in the liver but inhibited its activity in the kidney. There was no significant change in ACP activity in the liver of the CA32 group. Conversely, levels in the CA64 group were highest on day 4. Kidney ACP activity was lowest on day 1 and peaked on day 7 in the CA32 group, but was lowest after 12 h in the CA64 group. Both liver and kidney AKP activity increased with increasing exposure time. Liver AKP activity peaked on day 1 and 3 in the CA32 and CA64 groups, respectively. Our results suggest that liver and kidney SOD, ACP, and AKP play important role in the acclimation of G. przewalskii to carbonate alkalinity stress. The activity of these three enzymes was up-regulated by exposure to carbonate alkalinity stress, but recovered to control levels within 4 d, suggesting that G. przewalskii has the ability to adapt to concentrations 〈64 mmol/L carbonate alkalinity. The changes in the activity of these three enzymes likely plays an important role in protecting G. przewalskii from carbonate alkalinity stress. The activity of the three enzymes was up-regulated earlier in the kidney than in the liver, suggesting that the physiological responses to carbonate alkalinity occur earlier in the kidney than in the liver. Our results provide insight into how these three enzymes participate in the response of G. przewalskii to carbonate alkalinity stress, and provide a basis for setting water quality guidelines for the conservation of G. przewalskii.