多氯联苯(PCB153)对湛江叉鞭金藻生理生态和超微结构的影响

Effects of polychlorinated biphenyls (PCB153) on the physiological ecology and ultrastructure of Dicrateria zhanjiangensis

关键词:  湛江叉鞭金藻  六氯联苯PCB153  光合色素  超氧化物歧化酶  丙二醛  谷胱甘肽S-转移酶  超微结构

Key words:  Dicrateria zhanjiangensis  PCB153  Photosynthetic pigment  Superoxide dismutase  Malondialdehyde  Glutathione S-transferase  Ultrastructure

摘要:

为研究多氯联苯对海洋微藻的生理生态毒性，以湛江叉鞭金藻(Dicrateria zhanjiangensis)为研究对象，进行7 d的六氯联苯(PCB153)胁迫实验，比较其生长、光合色素含量、谷胱甘肽S-转移酶(GST)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量以及藻细胞超微结构的变化情况。结果显示，PCB153胁迫对湛江叉鞭金藻的生长、光合色素含量及抗氧化和解毒相关指标均有显著影响(P<0.05)。随着PCB153浓度的增大，其对湛江叉鞭金藻生长抑制作用不断增大，250 μg/L胁迫组藻细胞在第5天全部死亡。PCB153胁迫后，湛江叉鞭金藻叶绿素a、叶绿素c、类胡萝卜素和总光合色素均显著下降(P<0.05)，且随着PCB153浓度的增加，各实验组光合色素含量下降比例增大。PCB153胁迫后，各胁迫组藻细胞MDA含量显著增加；低浓度PCB153 (< 25 μg/L)胁迫显著诱导SOD和GST活性的提高；而高浓度PCB153(> 25 μg/L)胁迫则显著抑制2种酶活性。短期低浓度PCB153胁迫会改变金藻细胞超微结构，使细胞器形态改变、聚缩；高浓度PCB153胁迫则会直接破坏细胞膜的完整性，使细胞破裂，导致细胞自溶死亡。研究表明，PCB153抑制叉鞭金藻的生长和光合色素合成，低浓度PCB153激活抗氧化和解毒系统，提高其自我保护水平，高浓度PCB153加剧脂质过氧化，破坏抗氧化和解毒系统正常功能，导致细胞破裂死亡。

Abstract:

In order to study the physiological and ecological toxicity of polychlorinated biphenyls (PCBs) of marine microalgae, the growth, photosynthetic pigment content, glutathione S-transferase (GST), superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, and ultrastructure of Dicrateria zhanjiangensis were compared over 7 days under 2,2ʹ,4,4ʹ,5,5ʹ-hexachlorobiphenyl (PCB153) stress. The results showed that PCB153 stress had significant effects on the growth, photosynthetic pigment content, antioxidant and detoxification related indexes of D. zhanjiangensis (P<0.05). Increasing PCB153 concentration increased the inhibition of PCB153 on the growth of D. zhanjiangensis. In the 250 μg/L stress group, all the algae cells died on day five. The content of chlorophyll a, chlorophyll c, carotenoid, total light, and pigment had decreased significantly after the PCB153 stress (P<0.05). The decreasing photosynthetic pigment level was enhanced by the increase in PCB153 concentration. The MDA content of algal cells in all stress groups increased after the PCB153 stress. SOD and GST enzyme activities were significantly increased by low concentration PCB153 (<25 μg/L). Both enzyme activities were significantly inhibited by high concentrations of PCB153 (>25 μg/L). Under short-term low concentrations of PCB153 stress, the ultrastructure of the cells changed. To be specific, the organelle morphology altered and shrunk. Under high concentrations of PCB153 stress, the integrity of the cell membrane was destroyed, leading to cell rupture, autolysis and death. PCB153 can inhibit the growth and synthesis of photosynthetic pigments of D. zhanjiangensis. Low concentrations of PCB153 can activate the antioxidant and detoxification system. This activation improves self-protection capabilities. High concentrations of PCB153 can aggravate lipid peroxidation and destroy the normal function of antioxidant and detoxification systems, causing cell rupture and death.