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Biomedical subjects

J Wolff

Publications and source records attributed to J Wolff.

At least 289 records · Page 16Linked to original sources
PubMed1970

The effect of a purified preparation of lecithinase C on iodide transport.

Treatment of porcine thyroid slices with highly purified lecithinase C leads to a marked reduction in the ability to accumulate iodide ion. Although this response is less sensitive as a function of lecithinase concentration than is the ability to respond to thyrotropin with an increase in glucose oxidation, phospholipid synthesis or adenyl cyclase activity, it occurs when the baseline values of these parameters are not substantially altered.

Journal Article↗
PubMed1970

Hefe-phosphofructokinase: Reversible molekulare umwandlung und aufbau aus subeinheiten.

Yeast phosphofructokinase exists in several enzymically active, interconvertible forms with molecular weights of 180,000, 370,000, 570,000 and 750,000. With disc-electrophoresis catalytically active aggregation products with molecular weights of more than one million can be detected.In alkaline media fragmentation of phosphofructokinase occurs, leading to a variety of catalytically inactive products. These seem to be oligomers of subunits with 60,000 daltons. A model of the complex subunit structure of yeast phosphofructokinase is suggested. The various catalytically active forms of the enzyme are considered as polymers of 180,000 monomers, which themselves are enzymatically active and which are composed of three 60,000 subunits.

Journal Article↗
PubMed1970

Inhibition of hormone-sensitive adenyl cyclase by phenothiazines.

Chlorpromazine (3 x 10(-4)M) prevents the stimulation of adenyl cyclase activity in thyroid membranes produced by thyrotropin and prostaglandin, ACTH stimulation of adenyl cyclase in adrenal tissue, and glucagon- and epinephrine-stimulation of adenyl cyclase activity in liver. Baseline activity is unaffected. Parathyroid hormone stimulation of kidney preparations was not inhibited under these conditions. At chlorpromazine concentrations >3 x 10(-4)M F(-)-stimulated cyclase activity of thyroid and adrenal tissue was increased. Other phenothiazines, trifluoperazine, and prochlorperazine, have similar effects on thyrotropin and F(-)-stimulated cyclase activity of thyroid. Na(+)- K(+)-dependent ATPase of thyroid is also inhibited by chlorpromazine. Since thymol causes a similar dissociation of hormone- and F(-)-stimulated adenyl cyclase, it is concluded that the surface properties of these agents best account for their effects on adenyl cyclase.

Adenine Nucleotides↗
PubMed1970

Possible role of microtubules in thyroid secretion.

Colchicine and other microtubule-active agents have been found to block the release, stimulated by either thyroid-stimulating hormone or by dibutyryl cyclic adenosine 3':5'-monophosphate, of (131)I from previously (131)I-labeled mouse thyroid glands in vitro. The time and concentration characteristics of these inhibitors are consistent with their actions on microtubules in other systems. [(3)H]colchicine was also shown to be bound to a soluble 6S protein of bovine thyroid slices similar to the protein identified in other systems as a microtubular subunit. The demonstrated inhibition of colloid droplet formation and absence of an effect on thyroidal adenyl cyclase or cyclic 3':5'-phosphodiesterase suggests a colchicine-sensitive role for microtubules in colloid endocytosis in the thyroid gland.

Adenylyl Cyclases↗
PubMed1970

Antithyroid effects of lithium.

Lithium has been reported to be goitrogenic when used for the treatment of manic-depressive psychosis. To investigate the effects of lithium on iodine metabolism, male Sprague-Dawley rats were placed on a low iodine (LID) or normal iodine diet (NID) containing enough Li(2)CO(3) to give serum lithium levels of 0.23-0.86 mEq/liter (human therapeutic range is 0.6-1.6 mEq/liter). The following effects were noted with lithium treatment: (a) thyroid weight increased concomitant with a slowing of thyroidal iodine release; (b) the ability to concentrate iodide was increased only after goiters were established; (c) on the LID, (131)I uptake was elevated throughout all phases of treatment, even when the release rate was normal; (d) iodine organification was unaffected but the proportion of (131)I present as iodothyronines was decreased; (e) the thyroidal (127)I content was increased; (f) despite these changes, the serum PBI remained normal as did the thyroxine turnover rate; and (g) thyrotropin (TSH) levels in serum were the same as controls except for a slight elevation early in the course of treatment; TSH levels did not correlate with goitrogenesis. When LiCl was injected in large doses into intact rats (giving serum lithium levels of 3.08-3.89 mEq/liter), the iodide concentrating mechanism, (131)I uptake, and (131)I release rates were depressed. Similar experiments in hypophysectomized rats receiving TSH demonstrated these to be local antithyroid effects not mediated through the pituitary. The discrepancy between acute and chronic responses to lithium, and the dissociation between the inhibition of iodine release and stimulatory effects is discussed.

Animals↗