Centro de Investigacion en Alimentacion y Desarrollo, A.C., (CIAD), Carretera Gustavo Enrique Astiazaran Rosas 46, 83304, Hermosillo, Sonora, Mexico.
Department of Scientific and Technological Research, Universidad de Sonora (DICTUS), 83000, Hermosillo, Sonora, Mexico.
J Comp Physiol B. 2021 Jul;191(4):629-644. doi: 10.1007/s00360-021-01369-7. Epub 2021 Apr 24.
In most eukaryotic organisms, mitochondrial uncoupling mechanisms control ATP synthesis and reactive oxygen species production. One such mechanism is the permeability transition of the mitochondrial inner membrane. In mammals, ischemia-reperfusion events or viral diseases may induce ionic disturbances, such as calcium overload; this cation enters the mitochondria, thereby triggering the permeability transition. This phenomenon increases inner membrane permeability, affects transmembrane potential, promotes mitochondrial swelling, and induces apoptosis. Previous studies have found that the mitochondria of some crustaceans do not exhibit a calcium-regulated permeability transition. However, in the whiteleg shrimp Litopenaeus vannamei, contradictory evidence has prevented this phenomenon from being confirmed or rejected. Both the ability of L. vannamei mitochondria to take up large quantities of calcium through a putative mitochondrial calcium uniporter with conserved characteristics and permeability transition were investigated in this study by determining mitochondrial responses to cations overload. By measuring mitochondrial swelling and transmembrane potential, we investigated whether shrimp exposure to hypoxia-reoxygenation events or viral diseases may induce mitochondrial permeability transition. The results of this study demonstrate that shrimp mitochondria take up large quantities of calcium through a canonical mitochondrial calcium uniporter. Neither calcium nor other ions were observed to promote permeability transition. This phenomenon does not depend on the life cycle stage of shrimp, and it is not induced during hypoxia/reoxygenation events or in the presence of viral diseases. The absence of the permeability transition phenomenon and its adaptive meaning are discussed as a loss with biological advantages, possibly enabling organisms to survive under harsh environmental conditions.
在大多数真核生物中，线粒体解偶联机制控制着 ATP 合成和活性氧物质的产生。其中一种机制是线粒体内膜的通透性转换。在哺乳动物中，缺血再灌注事件或病毒疾病可能导致离子紊乱，如钙超载；这种阳离子进入线粒体，从而引发通透性转换。这种现象会增加内膜通透性、影响跨膜电位、促进线粒体肿胀，并诱导细胞凋亡。先前的研究发现，一些甲壳类动物的线粒体不存在钙调节的通透性转换。然而，在凡纳滨对虾 Litopenaeus vannamei 中，矛盾的证据阻止了这一现象的确认或否定。本研究通过测定线粒体对阳离子超载的反应，研究了凡纳滨对虾线粒体是否具有摄取大量钙的能力，以及是否存在通透性转换。通过测量线粒体肿胀和跨膜电位，我们研究了虾类是否会因缺氧再氧化事件或病毒疾病而导致线粒体通透性转换。本研究的结果表明，虾线粒体通过一个具有保守特征的典型线粒体钙单向转运体摄取大量的钙。钙和其他离子都没有观察到促进通透性转换。这种现象不依赖于虾的生命周期阶段，也不会在缺氧/复氧事件或存在病毒疾病时发生。讨论了通透性转换现象的缺失及其适应意义，认为这是一种具有生物学优势的丧失，可能使生物体能够在恶劣的环境条件下生存。
