Canesi L, Ciacci C, Piccoli G, Stocchi V, Viarengo A, Gallo G
Istituto di Anatomia e Fisiologia, Crocicchia, Urbino, Italy.
Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998 Aug;120(2):261-8. doi: 10.1016/s0742-8413(98)10004-x.
Hexokinase (E.C. 2.7.1.1), the enzyme responsible for glucose phosphorylation to G-6P, is inactivated by SH reagents and oxyradicals, and its inhibition has been involved in heavy metal toxicity in mammalian systems. In this work, the possibility that hexokinase activity could be affected by both heavy metal binding and oxidative stress conditions also in mussel tissues (Mytilus galloprovincialis Lam.) was investigated. The results obtained in vitro demonstrate that heavy metals inhibited digestive gland hexokinase (with Cd2+ > Cu2+ > Hg2+ > Zn2+ > Pb2+) and suggest a role for GSH in the protection against the heavy metal effects. Hexokinase activity was also reduced by addition of iron/ascorbate, indicating a susceptibility of the enzyme to metal-mediated oxyradical production. The effects of Cu2+ treatment (3 days, 40 micrograms l-1 per animal) on hexokinase activity and on the GSH/GSSG status were then evaluated in mussels exposed to a cycle of air exposure/reimmersion. In Cu-exposed mussels, a significant decrease in hexokinase activity and a parallel reduction in tissue GSH levels were observed, suggesting that the two effects of metal treatment could be related; however, hexokinase activity progressively recovered during air exposure and reimmersion, whereas the level of GSH showed a further decrease during air exposure followed by recovery after reimmersion. The in vitro results therefore indicate that mussel digestive gland hexokinase is susceptible to inactivation by heavy metal binding and suggest a role for GSH in the protection against the effects of heavy metals. The effects of copper were confirmed by the results obtained in vivo. The possible relationship between hexokinase activity and the level of GSH in the digestive gland of control and Cu-exposed mussels during air exposure and reimmersion are discussed, taking into account the balance between pro-oxidant and antioxidant processes at different stages of exposure.
己糖激酶（E.C. 2.7.1.1）负责将葡萄糖磷酸化为6-磷酸葡萄糖，它会被巯基试剂和氧自由基灭活，其抑制作用与哺乳动物系统中的重金属毒性有关。在本研究中，还调查了在贻贝组织（Mytilus galloprovincialis Lam.）中己糖激酶活性是否会受到重金属结合和氧化应激条件的影响。体外实验结果表明，重金属抑制消化腺己糖激酶（Cd2+ > Cu2+ > Hg2+ > Zn2+ > Pb2+），并表明谷胱甘肽（GSH）在抵御重金属影响方面发挥作用。添加铁/抗坏血酸也会降低己糖激酶活性，表明该酶对金属介导的氧自由基产生敏感。然后评估了Cu2+处理（3天，每只动物40微克/升）对暴露于空气暴露/再浸没循环的贻贝中己糖激酶活性和GSH/GSSG状态的影响。在暴露于铜的贻贝中，观察到己糖激酶活性显著下降，组织GSH水平平行降低，表明金属处理的这两种效应可能相关；然而，己糖激酶活性在空气暴露和再浸没过程中逐渐恢复，而GSH水平在空气暴露期间进一步下降，再浸没后恢复。因此，体外实验结果表明贻贝消化腺己糖激酶易受重金属结合的失活影响，并表明GSH在抵御重金属影响方面发挥作用。体内实验结果证实了铜的作用。考虑到不同暴露阶段促氧化和抗氧化过程之间的平衡，讨论了对照贻贝和暴露于铜的贻贝在空气暴露和再浸没期间消化腺中己糖激酶活性与GSH水平之间的可能关系。
