CELL MEMBRANE MICROVISCOSITY
CELL MEMBRANE MICROVISCOSITY
批准号:
3942060
负责人:
R KNAZEK
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至
中文摘要
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英文摘要
Change in the microviscosity of cell membranes were shown to
modulate the functionality of their receptors, presumably by
altering their ability to reorient into more or less active positions.
1) The abnormal accumulation of saturated long chain fatty acids
in the inherited disease of adrenoleukodystrophy also result in
stiff membranes for when human adrenocortical cells are cultured
in their presence, 15 times more ACTH is needed to achieve level
of cortisol synthesis. This probably explains the mechanism by
which adrenal insufficiency occurs in this disease. 2) Gossypol is
a dietary phenolic that has caused outbreaks of infertility in
several provinces in china. This compound causes an increase in
granulosa cell membrane microviscosity and thereby decreases
their estrogen response to FSH. Altered functionality of
gonadotropin receptors on target tissues is a likely mechanism by
which this phenomenon of infertility occurs. 3) We have shown
that the unique 19OH prostaglandins in human semen suppress
lymphocytes' response to mitogens 30 times more than PGE2.
Preliminary studies demonstrated that they reduce the
microviscosity of human lymphocyte membranes, a phenomenon
that may be extremely important in explaining the increased
susceptability of homosexuals to various infective agents. Other
preliminary studies have shown that these same prostaglandins
cause a marked decrease in the microviscosity of human
membranes, an observation that may be relevant to their role in
male reproductive physiology. A direct link between the immune
surviellance system and the adrenal gland was established when
human monocytes were shown to elaborate a soluble factor that
stimulates human adrenocortical cells to synthesize cortisol in
vitro. Preliminary studies have indicated that the monocytes and
granulocytes of diabetic patients metabolize arachidonic acid in
an abnormal fashion. The identity of these metabolites is being
established and the possible role in the microvascular disease of
diabetes is being studied.
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