X-Message-Number: 13197
Date: Fri, 4 Feb 2000 13:36:02 -0800 (PST)
From: Doug Skrecky <>
Subject: new cell dessication methods

    I'd like to thank Brent Thomas for posting the trehalose article.
This has been a long time in coming. It has been known for many years
that accumulation of intracellular trehalose (or sucrose) is critical for 
small animals as well as plants to survive complete dessication. The
methods for permeabilizing cells so as to allow large solutes to pass
through cell membranes have also been known for years. I'm glad to hear
these two areas of knowledge have finally been brought together to 
acheive some success.
    The only problem blocking the the achievement of reversible organ
cryopreservation is cryoprotectant toxicity. Large amounts of toxic
solutes like dmso, glycerol, and ethylene glycol kill cells through
various not-well-understood mechanisms. Perhaps this is a case of less
being more. A small amount of cryoprotectant combined with dessication
might achieve the goal of organ vitrification that some cryobiologists
have been searching for, for so many years.
    Below is an interesting article on glycerol.
---------- Forwarded message ----------

  Shen B.  Hohmann S.  Jensen RG.  Bohnert aH.
  Department of Plant Sciences, The University of Arizona, Tucson 85721, USA.
  Roles of sugar alcohols in osmotic stress adaptation. Replacement of glycerol
  by mannitol and sorbitol in yeast.
  Plant Physiology.  121(1):45-52, 1999 Sep.
  For many organisms there is a correlation between increases of metabolites
  and osmotic stress tolerance, but the mechanisms that cause this protection
  are not clear. To understand the role of polyols, genes for bacterial
  mannitol-1-P dehydrogenase and apple sorbitol-6-P
  dehydrogenase were introduced into a Saccharomyces cerevisiae mutant
  deficient in glycerol synthesis. Sorbitol and mannitol
  provided some protection, but less than that generated by a similar
  concentration of glycerol generated by glycerol-3-P dehydrogenase (GPD1).
  Reduced protection by polyols suggested that glycerol had specific functions
  for which mannitol and sorbitol could not substitute, and
  that the absolute amount of the accumulating osmoticum might not be crucial.
  The retention of glycerol and mannitol/sorbitol,
  respectively, was a major difference. During salt stress, cells retained more
  of the six-carbon polyols than glycerol. We suggest that the loss of >98% of
  the glycerol synthesized could provide a safety valve that dissipates
  reducing power, while a similar high intracellular concentration of retained
  polyols would be less protective. To understand the role of glycerol in salt
  tolerance, salt-tolerant suppressor mutants were isolated from the
  glycerol-deficient strain. One mutant, sr13, partially suppressed the
  salt-sensitive phenotype of the glycerol-deficient line, probably due to a
  doubling of [K(+)] accumulating during stress. We compare these results to
  the "osmotic adjustment" concept typically applied to accumulating
  metabolites in plants. The accumulation of polyols may have dual functions:
  facilitating osmotic adjustment and supporting redox control.

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