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Biomedical subjects

D H Nelson

Publications and source records attributed to D H Nelson.

At least 37 records · Page 2Linked to original sources
PubMed1979

Dexamethasone effect on the phospholipid content of isolated fat cell ghosts from adrenalectomized rats.

The lipid composition of sonicated ghosts from isolated fat cells has been investigated. Epididymal fat cells from adrenalectomized rats were incubated with and without 8 x 10(-8) M dexamethasone for 3 h. Phospholipids and cholesterol were isolated from membrane ghosts prepared from these cells. There was a 61% increase in membrane sphingomyelin from cells incubated with dexamethasone (P less than 0.025). No significant change was observed in other phospholipids, cholesterol, or fatty acid components of the phospholipids.

Adipose Tissue↗
PubMed1978

An effect of corticosteroids and 100% oxygen on aryl hydrocarbon hydroxylase, cytochrome-c reductase, and free radical formation by rat lung microsomes.

Activity of aryl hydrocarbon hydroxylase (AHH), cytochrome c-reductase, and NADPH oxidase, and epinephrine oxidation to adrenochrome were determined in lung microsomes from intact, adrenalectomized, and adrenalectomized cortisol-treated female rats under ambient and hyperoxic conditions. Microsomal adrenochrome formation, which is initiated by superoxide anion or other free radicals, was increased by adrenalectomy and decreased by cortisol treatment. Exposure of animals to 100% oxygen caused a further increase in adrenochrome formation. NADPH-cytochrome c-reductase and AHH activities were increased in incubations of microsomes from animals which had received cortisol in vivo while adrenalectomy led to decreases activity. NADPH oxidase activity was increased by cortisol in lung microsomes in the presence of either epinephrine or cytochrome c. Epinephrine conversion to adrenochrome in the presence of lung microsomes was blocked by SOD, but NADPH-cytrochrome c-reductase and AHH activity were unaffected.

Adrenalectomy↗
PubMed1978

Inhibition of leukocyte superoxide anion production by cortisol administration to normal subjects.

Superoxide anion production was suppressed in leukocytes obtained at two or four hours following oral administration of 50 to 100 mg of cortisol to normal subjects. The suppression lasted at least 4 hours but was not present at 24 hours. The measurement of superoxide anion production by leukocytes appears to be a convenient method for the serial estimation of an important biologic effect of corticosteroids in human subjects.

Cytochrome c Group↗
PubMed1977

Plasma ACTH levels in stressed and nonstressed adrenalectomized rats.

Following adrenalectomy there is a triphasic response of ACTH secretion characterized by an initial high rise immediately following the adrenalectomy, secondary to the stress of the procedure. This is followed by a fall to resting ACTH secretion until a steady state is reached 1 to 2 weeks following adrenalectomy at levels about 10 times normal. The ability to respond to stress with increased ACTH secretion is not lost at any time following adrenalectomy.

Adrenalectomy↗
PubMed1975

Corticosteroids increase superoxide anion production by rat liver microsomes.

Superoxide anion production by liver microsomes from intact, adrenalectomized, and cortisoltreated adrenalectomized rats has been determined. The amount formed was roughly proportionate to the amount of cortisol given, and a similar response was seen in the activity of NADPH-cytochrome c reductase. The amount of measurable superoxide anion was markedly reduced by the addition of superoxide dismutase. The increased production of this potent free radical with cortisol therapy suggests that its formation may contribute to some of the harmful effects of corticosteroids given in more than physiologic amounts.

Adrenalectomy↗