On the Oxidative Metabolism of the Rat Skin during Carcinogenesis induced by 7,12-dimethylbenz[a]anthracene

1966 ◽  
Vol 52 (4) ◽  
pp. 283-293
Author(s):  
Salvatore Di Bella ◽  
Umberto Pinchierri ◽  
Gabriella Richetta

The oxidation rate of citrate, d,1-isocitrate, glucose-6-phosphate and phosphogluconate proceeded two fold more rapidly in slices of rat skin with tumors induced by 7,12-dimethylbenz[a]anthracene than in normal skin. Citrate oxidation was stimulated by addition either of Fe++ or of cysteine, which, when both present in the system, are able to avoid the aconitase inactivation in the tissue. Mn++, NADP, FMN and cytocrome c may activate the oxygen uptake both in normal and pathological tissues, using as substrates respectively citrate, d,1-isocitrate, glucose-6-phosphate or phosphogluconate. The isocitric-dehydrogenase activity of the extracts of tumor induced rat skin resulted lower than that observed in normal rat skin; glucose-6-phosphate and respectively phosphogluconate-dehydrogenase enzymatic levels were two fold higher in the neoplastic than in the normal skin rat extracts. The results presented show an increase of the oxidative carbohydrate metabolism and pentosephosphate shunt, during carcinogenesis in the rat skin.

1980 ◽  
Vol 84 (3) ◽  
pp. 467-471
Author(s):  
N. DESHPANDE ◽  
IRENE MITCHELL

The effects of administration of testosterone propionate on the activities of seven of the enzymes of carbohydrate metabolism in normal rat mammary glands were investigated and the validity of the results was confirmed by simultaneous injection of the hormone and cyproterone acetate. The administration of the androgen increased the activities of phosphofructokinase (PFK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and lactate dehydrogenase (LDH) in glands from both intact and from ovariectomized and adrenalectomized animals. Administration of cyproterone acetate alone resulted in a significant reduction in the activities of PFK and G6PDH and when given together with the androgen it inhibited increases in the activities of PFK, G6PDH, 6PGDH and LDH induced by testosterone. It was concluded that these results did not explain the known inhibitory effects of the androgen on normal mammary gland growth and function.


2013 ◽  
Vol 135 (10) ◽  
Author(s):  
Clare Y. L. Chao ◽  
Gabriel Y. F. Ng ◽  
Kwok-Kuen Cheung ◽  
Yong-Ping Zheng ◽  
Li-Ke Wang ◽  
...  

An evaluation of wound mechanics is crucial in reflecting the wound healing status. The present study examined the biomechanical properties of healing rat skin wounds in vivo and ex vivo. Thirty male Sprague-Dawley rats, each with a 6 mm full-thickness circular punch biopsied wound at both posterior hind limbs were used. The mechanical stiffness at both the central and margins of the wound was measured repeatedly in five rats over the same wound sites to monitor the longitudinal changes over time of before wounding, and on days 0, 3, 7, 10, 14, and 21 after wounding in vivo by using an optical coherence tomography-based air-jet indentation system. Five rats were euthanized at each time point, and the biomechanical properties of the wound tissues were assessed ex vivo using a tensiometer. At the central wound bed region, the stiffness measured by the air-jet system increased significantly from day 0 (17.2%), peaked at day 7 (208.3%), and then decreased progressively until day 21 (40.2%) as compared with baseline prewounding status. The biomechanical parameters of the skin wound samples measured by the tensiometer showed a marked reduction upon wounding, then increased with time (all p < 0.05). On day 21, the ultimate tensile strength of the skin wound tissue approached 50% of the normal skin; while the stiffness of tissue recovered at a faster rate, reaching 97% of its prewounded state. Our results suggested that it took less time for healing wound tissues to recover their stiffness than their maximal strength in rat skin. The stiffness of wound tissues measured by air-jet could be an indicator for monitoring wound healing and contraction.


1965 ◽  
Vol 209 (5) ◽  
pp. 913-918 ◽  
Author(s):  
Francis J. Klocke ◽  
Gerard A. Kaiser ◽  
John Ross ◽  
Eugene Braunwald

The relative roles of augmented hemodynamic performance and direct stimulation of oxidative metabolism in mediating the increase of myocardial oxygen uptake (MVo2) produced by catecholamines have been examined in an isolated canine heart preparation. The responses of MVo2 to graded doses of isoproterenol, norepinephrine, or epinephrine were determined before and after the induction of cardiac arrest with potassium. Although increases of MVo2 occurred in the arrested state with the larger doses of the amines, they constituted only a small fraction, generally between 5 and 20%, of the increases produced by the same doses of amines when the hearts were beating. It is concluded that while large doses of catecholamines can increase oxidative metabolism of the nonbeating heart by a small amount, the increases of MVo2 produced by catecholamines in the beating heart are due in large part to the hemodynamic alterations which the amines induce.


2011 ◽  
Vol 111 (9) ◽  
pp. 2063-2068 ◽  
Author(s):  
Corey A. Rynders ◽  
Siddhartha S. Angadi ◽  
Nathan Y. Weltman ◽  
Glenn A. Gaesser ◽  
Arthur Weltman

Steroids ◽  
2009 ◽  
Vol 74 (9) ◽  
pp. 725-729 ◽  
Author(s):  
Agnes Mondok ◽  
Ibolya Varga ◽  
Edit Glaz ◽  
Nikolette Szucs ◽  
Miklós Tóth ◽  
...  

2019 ◽  
Vol 26 (9) ◽  
pp. 1306-1314.e5 ◽  
Author(s):  
Haoxin Li ◽  
Maria Ericsson ◽  
Bokang Rabasha ◽  
Bogdan Budnik ◽  
Sze Ham Chan ◽  
...  

1961 ◽  
Vol 200 (1) ◽  
pp. 34-38 ◽  
Author(s):  
Guy M. McKhann ◽  
Olaf Mickelsen ◽  
Donald B. Tower

Pyridoxine deficiency was produced in weanling kittens by dietary means. Clinically, the deficient animals showed failure to gain weight, ataxia, and, if left on the diet, seizures and death. In vitro study of isolated cerebral cortex slices from the deficient animals showed decreased formation of γ-aminobutyric acid and decreased oxygen uptake when glucose was the substrate. Addition of pyridoxal phosphate to the incubation media corrected both of these defects toward the levels found in normal littermate controls. The decreased oxygen uptake was also corrected by the addition of γ-aminobutyric acid to the media. It is suggested that in pyridoxine deficiency, cerebral oxidative metabolism is impaired by blockage of the γ-aminobutyric acid ‘shunt’ pathway at the glutamic decarboxylase step. The role of this shunt pathway in normal neuronal metabolism is discussed.


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