Search PubMed⌕ Search

Biomedical subjects

T R Tephly

Publications and source records attributed to T R Tephly.

At least 127 records · Page 7Linked to original sources
PubMed1977

Methyl alcohol poisoning III. Ocular toxicity.

The ocular toxicity of methyl alcohol has been investigated in six rhesus monkeys. All the animals developed fundus changes within 43 to 171 hours after its ingestion. The only fundus lesion seen was optic disc edema and associated changes, usually of a marked degree. Fluorescein fundus angiography confirmed the findings. The retinal and choroidal circulations, including the retinal capillary bed, were normal. Ophthalmoscopically and angiographically, optic disc edema in methyl alcohol poisoning was indistinguishable from that seen in raised intracranial pressure, except that no increased intracranial pressure was observed. It is postulated that optic disc edema in methyl alcohol poisoning is due to an axoplasmic flow stasis.

Animals↗
PubMed1977

Methyl alcohol poisoning. IV. Alterations of the morphological findings of the retina and optic nerve.

The ocular morphological findings of three methyl alcohol-intoxicated rhesus monkeys with optic disc swelling was investigated with light and electron microscopy in conjunction with intravascular horse radish peroxidase. Alterations observed in the optic nerve head were confined to the axons and consisted of swelling and clustering of the mitochondria, disruption of the neurotubules, the formation of vesicles, and enlargement of the axon segments in the prelaminar region. Swelling of the oligodendroglial cytoplasm in contact with the axons and of the astrocytes was seen in the retrolaminar optic nerve and the intraorbital optic nerve. Alterations were not observed in the retina. It is hypothesized that the alterations in the axons are the result of disrupted axoplasmic flow. Possible mechanisms relating methyl alcohol intoxication to disruption of axoplasmic flow are discussed.

Animals↗
PubMed1976

Delta-Aminolevulinic acid synthetase in the heart.

The regultion of cardiac delta-aminolevulinic acid synthetase activity was studied in rat heart homogenates. Optimal conditions were determined for the measurement of delta-aminolevulinic acid and an appropriate assay was established for the heart. The activity of cardiac delta-aminolevulinic acid synthetase was determined in rats either fed ad libitum or starved for 24 or 48 h. Marked decreases in delta-aminolevulinic acid synthetase activity were observed in homogenates or mitochondrial fractions prepared from hearts of fasted animals and an explanation for previous findings that the enzyme is undetectable in heart tissue is provided. Dexamethasone treatment was effective in reversing the decreases brought about by fasting but had no effect on the delta-aminolevulinic acid synthetase activity in heart homogenates from fed rats. ACTH treatment had no effect in fed or starved rats. Decreases in delta-aminolevulinic acid synthetase activity induced by fasting were not reversed in homogenates or mitochondrial preparations by succinyl-CoA-generating systems or when alpha-ketoglutarate was substituted for succinate in homogenate preparations. Cardiac delta-aminolevulinic acid dehydratase levels are not altered by fasting. Agents such as allylisopropylacetamide or 3,5-dicarbethoxy-1,4-dihydrocollidine, which produce marked increases in hepatic delta-aminolevulinic acid synthetase activity, have no effects on the activity of this enzyme in the heart.

5-Aminolevulinate Synthetase↗
PubMed1976

Studies on heme synthesis in the rat adrenal.

The activity and regulation of rat adrenal delta-aminolevulinic acid synthetase (EC 2.3.1.37) has been studied. The activity of delta-aminolevulinic acid synthetase in rat adrenal homogenates is comparable to the activity found in rat hepatic homogenates when untreated animals are employed. Starvation of rats for 24 and 48 hours increased adrenal delta-aminolevulinic acid synthetase activity without altering the hepatic enzyme. The treatment of rats with ACTH gel also increased adrenal delta-aminolevulinic acid synthetase activity. The effect of starvation on rat adrenal delta-aminolevulinic acid synthetase activity appears to be mediated by ACTH and can be prevented by the administration of dexamethasone. Adrenal delta-aminolevulinic acid synthetase appears to be refractory to induction by agents which induce the hepatic enzyme. These results suggest that the adrenal enzyme may be uniquely controlled by neural and endocrine influences which differ from the factors which regulate the activity of the hepatic enzyme.

5-Aminolevulinate Synthetase↗
PubMed1975

A possible role of copper in the regulation of heme biosynthesis through ferrochelatase.

Experiments have been performed which show that it is possible to regulate heme biosynthesis by regulating ferrochelatase activity. Treatment of rats with the transition metals, Co-++ and Mn-+-+, has been shown to inhibit ferrochelatase activity and to produce a dose-dependent decrease in hepatic cytochrome P-450 content. Unlike other transition metals, copper stimulated ferrochelatase activity and there was an interaction between Cu-+-+ and Fe-+-+ in the system such that the Km of Fe-+-+ was dependent on the concentration of copper. After solubilizing and dialyzing hepatic mitochondrial preparations, ferrochelatase activity was lost and could be restored by the addition of copper. In addition, copper, but not iron, reversed the inhibition of ferrochelatase activity produced by Pb-+-+ or Co-+-+. This study suggest that cytochrome P-450 content may be decreased during copper deficiency due to a decrease in ferrochelatase activity and a subsequent defect in heme biosynthesis. The synthesis of other hemoproteins may also be affected by copper deficiency. For example, it is well known that copper deficiency can lead to anemias (Lee et al., 1968) which might be explained by an intracellular defect in heme biosynthesis at ferrochelatase.

Animals↗