EFFECTS OF COLD, ASCORBIC ACID, AND AGE ON “FORMALDEHYDE-INDUCED” ARTHRITIS IN THE WHITE RAT

1951 ◽  
Vol 29 (2) ◽  
pp. 35-47
Author(s):  
Louis-Paul Dugal

Ascorbic acid has been claimed to have a definite antirheumatic activity in humans. It has also been found to have a slight protective action against experimental arthritis in animals. We have been able to show that ascorbic acid has a definite and significant beneficial effect on the same disease in adult rats, but not in young animals. Moreover, our results show that the formalde hyde-induced arthritis is greatly aggravated by exposure to cold.

1960 ◽  
Vol 38 (1) ◽  
pp. 175-185
Author(s):  
James Campbell ◽  
Gordon R. Green ◽  
Eduard Schönbaum ◽  
Harvey Socol

Exposure of adult rats to a cold environment increased the coenzyme A (CoA) extractable from their livers. The increases, in rats fed a complete diet, were found within 3 days, and were larger the longer the duration of exposure, amounting to 6, 27, and 60% above the control values after 3, 17, and 24 days respectively. The relations were similar when the CoA from the liver was expressed per unit weight of fresh tissue, or of liver total solids, or of whole body. When rats were fed a diet deficient in pantothenic acid, exposure to cold also resulted in elevation of CoA in the liver, but the differences did not progress with the duration of exposure. The liver CoA was further increased by the addition of large amounts of ascorbic acid to both the complete and the pantothenate-deficient diets. This effect of ascorbic acid occurred in rats under both ordinary and cold environmental conditions. Exposure to cold did not alter the concentration of CoA in the adrenal glands, but caused enlargement of the glands so that the amount of CoA in the adrenal per unit weight of the whole body increased. Other alterations in these animals exposed to cold included enlargement of the kidneys and heart, and decrease in depot fat. Deficiency of pantothenate in the diet slowed the rate of growth of young rats and significantly reduced the levels of CoA in the liver and the adrenal glands.


1960 ◽  
Vol 38 (2) ◽  
pp. 175-185 ◽  
Author(s):  
James Campbell ◽  
Gordon R. Green ◽  
Eduard Schönbaum ◽  
Harvey Socol

Exposure of adult rats to a cold environment increased the coenzyme A (CoA) extractable from their livers. The increases, in rats fed a complete diet, were found within 3 days, and were larger the longer the duration of exposure, amounting to 6, 27, and 60% above the control values after 3, 17, and 24 days respectively. The relations were similar when the CoA from the liver was expressed per unit weight of fresh tissue, or of liver total solids, or of whole body. When rats were fed a diet deficient in pantothenic acid, exposure to cold also resulted in elevation of CoA in the liver, but the differences did not progress with the duration of exposure. The liver CoA was further increased by the addition of large amounts of ascorbic acid to both the complete and the pantothenate-deficient diets. This effect of ascorbic acid occurred in rats under both ordinary and cold environmental conditions. Exposure to cold did not alter the concentration of CoA in the adrenal glands, but caused enlargement of the glands so that the amount of CoA in the adrenal per unit weight of the whole body increased. Other alterations in these animals exposed to cold included enlargement of the kidneys and heart, and decrease in depot fat. Deficiency of pantothenate in the diet slowed the rate of growth of young rats and significantly reduced the levels of CoA in the liver and the adrenal glands.


1962 ◽  
Vol 39 (3) ◽  
pp. 345-352
Author(s):  
H. BARNES

1. The results of some chemical analyses for inorganic and organic constituents of the seminal plasma of Balanus balanus are presented. 2. The inorganic ions show a cation deficit of 178 m-equiv./l., which is probably made up by free amino-acids. 3. Cystine is a prominent amino acid present. 4. Potassium and calcium are present in excess of their quantities in sea water. 5. Reducing sugars, compared with the amount found in sea-urchin spermatozoa, are found in moderate quantities, 1 mg./ml. 6. Phosphorus of all kinds is present in only small quantities (total of o.14 mg./ml.). 7. Some phosphatases are present. 8. There are 21 /µg./ml. of ascorbic acid; the function of this is discussed in relation to its possible contribution to the protective action against the poisoning of -SH groups by thiol-reactive agents.


1960 ◽  
Vol 199 (5) ◽  
pp. 847-850 ◽  
Author(s):  
S. M. McCann ◽  
S. Taleisnik

Luteinizing hormone (LH) depleted ovarian ascorbic acid of immature or adult rats pretreated with gonadotrophins, the former animals being more sensitive than the latter. Follicle-stimulating hormone, luteotrophin and adrenocorticotrophin had minimal or o activity in this assay, whereas vasopressin but not oxytocin had appreciable activity. Vasopressin was more active in the adult rats. If the doses were expressed on a weight basis, vasopressin was actually more potent than the LH standard in the adults; however, endogenous vasopressin release did not deplete ovarian ascorbic acid. The activity of both LH and vasopressin was either not affected or affected to the same degree by hypophysectomy. Retrograde injection of vasopressin into the ovarian vein showed that the action of vasopressin was a direct one on the ovary. Vasopressin does not interfere with the assay of LH in body fluids by this technique.


2006 ◽  
Vol 98 (5) ◽  
pp. 467-472 ◽  
Author(s):  
Surinder Kumar Yogeeta ◽  
Rao Balaji Raghavendran Hanumantra ◽  
Arunachalam Gnanapragasam ◽  
Senthilkumar Subramanian ◽  
Subhashini Rajakannu ◽  
...  

1951 ◽  
Vol 29 (4) ◽  
pp. 164-175
Author(s):  
O. Héroux ◽  
L.-Paul Dugal

In previously reported observations, we have shown that (a) ascorbic acid, given in large doses, had a hypotensive effect on normal blood pressure, (b) the initial hypotension, due to sudden exposure to cold, was prevented by large doses of ascorbic acid, (c) the hypertension encountered upon long exposures to cold was lowered by ascorbic acid. The present paper confirms the last result and also shows that actually ascorbic acid has a hypotensive action on experimental hypertension obtained by the two following ways: (1) excess of sodium chloride in drinking water and (2) renal compression. The hypertension and adrenal hypertrophy caused by a long exposure to cold regress when the animals are brought back to normal temperature. In its initial phase, the experimental renal hypertension is lowered by ascorbic acid but not in its chronic phase.


Hypertension ◽  
2000 ◽  
Vol 35 (4) ◽  
pp. 936-941 ◽  
Author(s):  
Debra L. Sherman ◽  
John F. Keaney ◽  
Elizabeth S. Biegelsen ◽  
Stephen J. Duffy ◽  
Jay D. Coffman ◽  
...  

1949 ◽  
Vol 27e (6) ◽  
pp. 349-363 ◽  
Author(s):  
M. Thérien ◽  
J. Leblanc ◽  
O. Héroux ◽  
L. P. Dugal

It has been shown recently by Dugal and Thérien that during a short or long exposure to cold, the normal hypertrophy of the adrenals is completely prevented by large doses of ascorbic acid, and that, nevertheless, at the same time, resistance is increased towards the same damaging agent. So, the most universally accepted criterion of damage caused by stress is abolished when the animals exposed to cold receive large doses of ascorbic acid. Starting from that observation, it was natural to wonder what would be the effects of the ascorbic acid on the biological changes normally associated with the hypertrophy of the adrenals during exposure to cold. The present paper describes the experimental studies made in that connection; the results obtained show that: (1) ascorbic acid (a) partly inhibits the thymus atrophy normally encountered upon exposure to any stress including cold, (b) accelerates in a very significant way the enlargement of the thyroid, (c) is responsible for an increase in weight of the spleen, whereas the control animals, on the contrary, show a decrease in weight of the same organ; (2) the histamine content of the adrenals, which increases at room temperature under the influence of ascorbic acid, is significantly decreased during exposure to cold under the influence of the same substance; (3) the activity of the adrenals, far from being inhibited by ascorbic acid is even increased if the cholesterol changes are taken as an index of that activity; (4) the initial hypotension—due to cold—found in our controls, is prevented by large doses of ascorbic acid; on the other hand, if hypertension develops after long exposure to cold, the subsequent administration of large doses of ascorbic acid restores the blood pressure to normal. Confirmation has also been obtained for the previously reported observation that ascorbic acid prevents the hypertrophy of the adrenals during exposure to cold.


2018 ◽  
Vol 43 (3) ◽  
pp. 19
Author(s):  
Juliana Metzner Franco ◽  
Silvana Marina Piccoli Pugine ◽  
Antônio Márcio Scatoline ◽  
Mariza Pires De Melo

The aim of the present study was to evaluate in vitro antioxidant capacity of Melissa extract (ME) (Melissa officinalis L.) and its protective effect on peroxyl radical-induced oxidative damage in erythrocytes. ME used in present study was obtained by rota-evaporation of the crude extract (ethanol:water/dried leaves). Total phenolic and flavonoids contend determination, 176.8 ± 13.2 mg GAE/g dw and  26.2 ± 3.2 mg QE/g dw, respectively).  Total equivalent antioxidant activities, TEAC in mg TE/g dw, were 61.4 ± 5.5 and 512.4 ± 77.2 for respective FRAP assay and DPPH• radical-scavenging. The ME acts as an antioxidant on NO and O2•-, when ME exerted a higher antioxidant action on NO scavenging to compared to the ascorbic acid (1.9 times), however, the antioxidant capacity of ME on O2•- was lower than ascorbic acid (5.6 times). The values of hemolysis inhibition from ME (IC50, 2.0 ± 0.5 mg/mL) were higher than ascorbic acid (IC50, 7.1 ± 1.8 mg/mL). Extract of Melissa was able to eliminate biological free radicals, suggesting a potential to prevent oxidative damage in vivo. In fact, the ME exerted protective action on cell membrane lysis in situ.


Sign in / Sign up

Export Citation Format

Share Document