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Biomedical subjects

J R Arthur

Publications and source records attributed to J R Arthur.

108 records · Page 6Linked to original sources
PubMed1979

Observations on the selenium status of cattle in the north-east of Scotland.

Cattle on 18 of 21 farms in north-east Scotland were found to have low whole blood activities of the selenium-containing enzyme, glutathione peroxidase (less than 5 units per ml whole blood), and a low blood concentration of selenium (less than 0.05 mg per litre). These cattle had all been fed on locally produced feedstuffs without any mineral supplementation. The low selenium status in cattle occurred on farms with soils derived from a range of parent material, no one particular type predominating.

Animals↗
PubMed1978

Control of sterol metabolism in rat adrenal mitochondria.

Steroidogenesis by adrenal mitochondria from endogenous precursors is stimulated by corticotropin (ACTH) and is sensitive to the protein-synthesis inhibitor cycloheximide. In the present investigation the effect of cycloheximide treatment on the metabolism of a number of analogues of the normal steroidogenic substrate, i.e. cholesterol, by rat adrenal mitochondria was studied. It was observed that the metabolism of analogues such as desmosterol, 26-norcholest-5-en-3beta-ol and 5-cholen-3beta-ol (that is with non-polar alkyl side chains like cholesterol), was sensitive to cycloheximide treatment. By contrast, the metabolism of those analogues with polar groupings on the side chain, i.e., 20alpha-, 24-, 25- and 26-hydroxycholesterols was insensitive to pretreatment with cycloheximide. The binding of added sterol to the cytochrome P-450 component of the mitochondrial sterol desmolase was studied. Similar studies on the equilibration time on addition of exogenous sterols to achieve maximum rates of pregnenolone production were also made. Both studies show that cholesterol, a non-polar sterol, penetrated slowly through the mitochondrial milieu to reach the cytochrome P-450 reaction centre whereas 24- and 26-hydroxycholesterols rapidly attained the enzymic environment. The cycloheximide-sensitive process in sterol metabolism appeared related to the transfer of non-polar sterols such as cholesterol within the mitochondria to a region in close proximity to the enzyme. The importance, and possible mechanism of action, of the cycloheximide-sensitive factor in the control of adrenal steroidogenesis is discussed.

Adrenal Glands↗
PubMed1978

Regulation of cholesterol metabolism in rat adrenal mitochondria.

Addition of cholesterol to rat adrenal mitochondria resulted in a stimulation of pregnenolone synthesis. The slow step of the mitochondrial cholesterol side-chain cleavage reaction could be the interaction of the sterol with cytochrome P-450. The rate of cholesterol binding to this enzyme as observed spectroscopically correlated with the equilibration period (20 min) of the mitochondria and exogenous cholesterol required for maximal rates of pregnenolone synthesis. It is suggested that translocation of cholesterol between different sterol pools occurs within the mitochondria. Potential intracellular effectors that could be of importance in the movement or regulation of mitochondrial cholesterol include bivalent metallic ions, prostaglandins, cyclic nucleotides, polyamines and polylysine. Of the effectors studied, only calcium ions and polylysine markedly stimulated pregnenolone synthesis. These effectors might stimulate steroidogenesis by lateral displacement of cholesterol in the mitochondrial membrane into a compartment easily accessible to the cholesterol side-chain cleavage enzyme complex.

Adrenal Glands↗
PubMed1976

Oxidation of cholesterol and cholesterol analogues by mitochondrial preparations of steroid-hormone-producing tissue.

The rate of oxidation of cholesterol and its analogues to pregnenolone (3beta-hydroxypregn-5-en-20-one) by various mitochondrial preparations was measured. Sterols with the cholest-5-en-3beta-ol ring system and saturated side chains of different lengths were converted into pregnenolone rat rates similar to that of cholesterol. This marked lack of mitochondrial specificity towards the steroid side chains is in direct contrast with the rat liver microsomal cholesterol 7alpha-hydroxylase, which has a high specificity for the side chain. Steroids that retain the ring system, but contain hydroxyl groups at various points in the side chain, are converted into pregnenolone at rates three to eight times higher than in cholesterol. The results are discussed with reference to current ideas on the mechanism of the side-chain cleavage of cholesterol. The results are discussed with reference to current ideas on the mechanism of the side-chain cleavage of cholesterol.

Adrenal Cortex↗
PubMedDate not supplied

The role of selenium in thyroid hormone metabolism and effects of selenium deficiency on thyroid hormone and iodine metabolism.

Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases, which convert thyroxine (T4) to the more metabolically active 3,3'-5 triiodothyronine (T3). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [125I]N-bromoacetyl reverse triiodothyronine, is also labeled with 75Se by in vivo treatment of rats with 75Se-Na2SeO3. Thus, the type I iodothyronine 5'-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent selenium deficiency could be a major determinant of the severity of iodine deficiency.

Animals↗
PubMedDate not supplied

Iodine deficiency in cattle: compensatory changes in thyroidal selenoenzymes.

The trace elements selenium and iodine are both essential for normal thyroid hormone metabolism. To investigate the relationships between these functions, heifers were maintained on iodine-deficient or iodine-sufficient diets from mid pregnancy to term. In these heifers and their offspring the interrelationship between iodine and selenium was apparent with the preferential 10- to 12-fold induction of the selenoenzyme, thyroidal type I, selenium-containing iodothyronine deiodinase activity by iodine deficiency. This was accompanied by two- to four-fold increases in cytosolic glutathione peroxidase activity, probably reflecting increased oxidative activity and metabolism in the thyroid gland in response to iodine deficiency. The above selenoenzyme activities were not affected in liver, kidney, pituitary and brain by iodine deficiency. The results are consistent with a critical role for selenium in both the normal function of cattle thyroid and key enzymes to compensate for the effects of iodine deficiency.

Animals↗
PubMedDate not supplied

Blood antioxidants and indices of lipid peroxidation in subjects with angina pectoris.

We tested the antioxidant hypothesis of coronary heart disease (CHD) by comparing blood antioxidants, indices of lipid peroxidation and classic (CHD) risk factors of 25 subjects with stable angina pectoris with 200 matched controls. Angina subjects had significantly increased plasma concentrations of total cholesterol, low density lipoproteins and triglycerides although body mass index, plasma cotinine concentration and blood pressure were similar to those of the control group. Plasma concentrations of vitamin A, vitamin C and cholesterol- adjusted vitamin E did not differ between the groups although subjects with angina had significantly decreased plasma uric acid concentrations and elevated indices of lipid peroxidation. Although the results are compatible with the antioxidant hypothesis, it is unclear whether the increased oxidative stress in angina sufferers is a cause or consequence of the disease.

Angina Pectoris↗