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There are three main types of cell death caused by ultra-low temperature preservation: cell rupture (associated with ice crystal production), cell necrosis, and apoptosis.
death caused by ultra-low temperature preservation are mainly of the following three types: cell rupture (associated with ice crystal production), cell necrosis, and apoptosis.
some studies have found that cell death caused by ultra-low temperature preservation is late on, and further research on the mechanisms behind late death suggests that this death is mainly caused by both cell necrosis and apoptosis.
, different from the passive process of cell necrosis, apoptosis, as an energy-related, gene-controlled way of autonomous and orderly cell death, has been widely concerned by researchers of ultra-low temperature preservation mechanism.
apoptosis is usually detected using parameters such as cysteine protease vitality, externalization of phosphatidylserine, changes in mitochondrial membrane position, and DNA fragmentation.
Paasch and others compared the effects of ultra-low temperature preservation on the apoptosis parameters of human sperm cells, and found that after ultra-low temperature preservation, the activity of cysteine proteases-3, -8 and -9 increased significantly, and the mitochondrial membrane potential decreased, but there was no significant change in DNA fragments.
Martin and others also found in ultra-low temperature preserved bovine sperm mitochondrial membrane possible reduction, cysteine protease activity and cell membrane permeability, and detected the production of cytochrome C and apoptosis induced factors, two proteins associated with apoptosis, but found no significant changes in DNA fragmentation and cell nucleation.
Vogel compared the ratio of mitochondrial proteins Bcl-XL and Bax in fibroblasts of human derma using immunoprinting techniques (the ratio of these two proteins represents the positive and negative ratios of apoptosis), and found a slight increase in the ratio after ultra-low temperature preservation of reheat, with a significant increase of 6 h and 12 h after that, until 24 h was restored to a level comparable to that of the control.
the genomes of mouse ovary follicles before and after ultra-low-temperature preservation, such as Liu, found that ultra-low-temperature preservation induced the expression of apoptosis genes Fas and Fass lipenses.
Park and others have also demonstrated that the freeze-thaw process causes increased expression of apoptosis-related survival, Fass, hot shock protein 70 and cysteine protease-3 in bovine blastocyst cells.
studies have shown a correlation between ultra-low temperature preservation and apoptosis, but also point the way to how to mitigate or eliminate the effects of apoptosis.
cysteine protease inhibitors have been shown to reduce the activity of cysteine protease-3 in ultra-low temperature preservation of pig liver cells, reduce the release of cytochrome C in mitochondria, slow down the decline of mitochondrial membrane levels, and significantly increase the functional indicators of liver cell vitality - albumin production, metabolism and urea production of dixie.
in the ultra-low temperature preservation of liver cells in rats, the addition of cysteine protease inhibitors significantly improved the differentiation and function of liver cells at 6 h and 24 h after reheating.
oxidative stress and apoptosis as the two major research hotspots of physiological phenomena in ultra-low temperature preservation in recent years, it is also inextricably linked.
studies have shown that Oxidative stress in ultra-low temperature preservation can not only directly cause cell damage, but also induce apoptosis, such as reactive oxygen activation nucleation transcription factor NF-B (nuclearfactor-kappa B, NF-B), leading to apoptosis;
apoptosis produced by mitochondria as shown in Figure 2 can reflect to some extent the relationship between apoptosis and oxidative stress in ultra-low temperature preservation.
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