Biomedical subjects

C Frenkel

Publications and source records attributed to C Frenkel.

47 records · Page 3Linked to original sources

PubMed1979

Effect of ethanol, acetaldehyde, acetic Acid, and ethylene on changes in respiration and respiratory metabolites in potato tubers.

Ethanol, acetaldehyde, and acetic acid, when applied in a volatile state in air to potato tubers, led to a climacteric-like upsurge in respiration. The respiratory upsurge was markedly enhanced when the volatiles were applied in 100% O(2).Ethanol induced a decline in the level of 2-phosphoglyceric acid and phosphoenolpyruvate while leading to the accumulation of tricarboxylic acid cycle intermediates including isocitrate and alpha-ketoglutarate. The action of these compounds was similar to, but independent of, the action of ethylene.

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PubMed1978

Cyanide-resistant Respiration in Freshly Cut Potato Slices.

Treating intact white potato (Solanum tuberosum L.) tuber with ethylene in air or O(2) made it possible to obtain freshly cut slices which exhibit cyanide-resistant respiration. The cyanide-resistant path requires induction in whole tubers. The data also indicate that high O(2) concentration is necessary for the full development of cyanide-resistant respiration.

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PubMed1977

Involvement of hydrogen peroxide in the regulation of senescence in pear.

Endogenous peroxide levels in pear fruit (Pyrus communis) were measured using a titanium assay method, and were found to increase during senescence in both Bartlett and Bosc varieties. Application of glycolic acid or xanthine, serving as substrates for the formation of H(2)O(2), increased the peroxide content of the tissue and accelerated the onset of ripening, as measured by increased softening and ethylene evolution. Application of ethylene also induced increased peroxide levels. Ripening processes were similarly promoted when peroxides were conserved by inhibiting the activity of catalase with hydroxylamine or potassium cyanide. By comparison, the inhibition of glycolate oxidase with alphahydroxy-2-pyridinemethanesulfonic acid decreased the peroxide content of the tissue and delayed the onset of ripening. These results indicate that the onset of ripening correlates with the peroxide content of fruit tissues as occurring under normal conditions or as influenced by the treatments. Hydrogen peroxide may be involved in oxidative processes required in the initiation and the promotion of ripening.

Journal Article↗

PubMed1977

Upsurge in respiration and peroxide formation in potato tubers as influenced by ethylene, propylene, and cyanide.

A continuous application of ethylene (10 mul/l) and propylene (500 mul/l) to potato tubers (Solanum tuberosum L.) resulted in an upsurge of respiration and a concomitant rise in peroxides. When applied in 100% O(2), the effect of ethylene and propylene on respiration and peroxide formation was augmented. Hydrogen cyanide (500 mul/l) mimicked the action of ethylene and propylene inducing a respiratory rise and a corresponding increase in peroxides. As with ethylene, the effect of HCN was augmented in high O(2) tensions. The results support the suggestion that ethylene activates the cyanide-insensitive respiratory pathway.

Journal Article↗

PubMed1975

Oxidative turnover of auxins in relation to the onset of ripening in bartlett pear.

Pears (Pyrus communis var. Bartlett) kept in 100% O(2) showed an increase in the rate of softening, chlorophyll degradation, and ethylene evolution. The O(2) application could overcome, in part, the inhibition of ripening by 1 mm indoleacetic acid. Ripening of pears was also accelerated by the application of solutions containing indoleacetic acid-oxidation products, obtained by an overnight incubation of 0.1 and 1 mm indoleacetic acid with traces of H(2)O(2) and horseradish peroxidase. Although both treatments stimulated ethylene evolution, the promotion of ripening could not be attributed to an indirect ethylene effect. Indoleacetic acid oxidation products obtained in vivo by high O(2) tensions or in vitro by enzymatic degradation may function in the promotion of fruit ripening and the synthesis of ethylene.

Journal Article↗

PubMed1975

Promotion of softening and ethylene synthesis in bartlett pears by 3-methylene oxindole.

A purified preparation of 3-methylene oxindole (3-MeOx) was applied to Bartlett pears (Lyrus communis) by vacuum infiltration. The infiltrated fruit were kept at room temperature at atmospheric or at one-twentieth of an atmospheric tension. The rate of softening was markedly enhanced by the application of 0.1 and 1 mum 3-MeOx. At 10 mum 3-MeOx the promotive effect of the compound was diminished. All the employed concentrations of 3-MeOx exceeded the effect of applied ethylene. The enhancement of softening in fruit kept under hypobaric conditions suggests that the action of 3-MeOx is a direct one and not an indirect ethylene effect. 3-MeOx also showed stimulation in the onset of ethylene synthesis, shortening the time required to obtain the peak in ethylene synthesis from 5 days by the control to 3 days by 0.1 mum and 2 days by 1 mum of the applied compound. As with softening, 3-MeOx at 10 mum diminished the rate of ethylene synthesis.The results suggest that 3-MeOx could function as a senescence promoter in fruit. Also, since auxins retard ripening while 3-MeOx promotes ripening, the action of 3-MeOx may be considered as that of an auxin antagonist. The occurrence and the mode of action of 3-MeOx as a possible senescence factor in fruit are discussed.

Journal Article↗

PubMed1973

Auxin inhibition of ripening in bartlett pears.

The effect of indoleacetic acid and 2,4-dichlorophenoxyacetic acid on the ripening of intact mature-green pears (Pyrus communis var. Bartlett) was investigated using a vacuum infiltration technique.The effects of indoleacetic acid and 2,4-dichlorophenoxyacetic acid at concentrations of 0.01, 0.1, and 1.0 mm each were studied on softening, degreening, and on ethylene and CO(2) evolution. Softening and degreening were inhibited increasingly in response to increased concentrations of indoleacetic acid. This inhibitory property was amplified by 2,4-dichlorophenoxyacetic acid at concentrations comparable to those of indoleacetic acid. Application of the auxins also prevented the climacteric rise in respiration, but stimulated ethylene synthesis. Despite the presence of elevated ethylene levels, the inhibitory auxin effect was predominant.It is proposed that endogenous auxins in fruit represent a resistance factor in ripening and must be inactivated before ripening can occur.

Journal Article↗

PubMed1973

Initiation of Ripening in Bartlett Pear with an Antiauxin alpha(p-Chlorophenoxy)isobutyric Acid.

A vacuum infiltration technique was used to apply an anti-auxin, alpha-(p-chlorophenoxy) isobutyric acid to mature green pears (Pyrus communis var. Bartlett). Application of alpha-(p-chlorophenoxy) isobutyric acid, at 0.02, 0.2, and 2.0 mm progressively accelerated the onset of chlorophyll degradation, softening, and CO(2) evolution. The action of alpha(p-chlorophenoxy) isobutyric acid is apparently independent of ethylene, since the auxin analogue depressed ethylene evolution and could overcome ethylene deficiency in fruit ripening under hypobaric conditions.The auxin analogue decreased the Michaelis constant of indoleacetic acid oxidase in vitro, suggesting that the antiauxin action of alpha-(p-chlorophenoxy) isobutyric acid is the acceleration in the breakdown of endogenous auxins in fruit and subsequently the initiation of ripening.

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PubMed1972

Involvement of Peroxidase and Indole-3-acetic Acid Oxidase Isozymes from Pear, Tomato, and Blueberry Fruit in Ripening.

Protein extracts were obtained from climacteric fruits (pear, tomato) and nonclimacteric fruits (blueberry) during various stages of ripening. The use of a gel electrophoresis technique revealed a consistent reinforcement in indoleacetic acid oxidase but not in peroxidase isozymes during ripening. The significance of the results is discussed in relation to the resistance of fruits to ripening and ethylene action.

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PubMed1968

Protein synthesis in relation to ripening of pome fruits.

Protein synthesis by intact Bartlett pear fruits was studied with ripening as measured by flesh softening, chlorophyll degradation, respiration, ethylene synthesis, and malic enzyme activity. Protein synthesis is required for normal ripening, and the proteins synthesized early in the ripening process are, in fact, enzymes required for ripening. (14)C-Phenylalanine is differentially incorporated into fruit proteins separated by acrylamide gel electrophoresis of pome fruits taken at successive ripening stages. Capacity for malic enzyme synthesis increases during the early stage of ripening. Fruit ripening and ethylene synthesis are inhibited when protein synthesis is blocked by treatment with cycloheximide at the early-climacteric stage. Cycloheximide became less effective as the climacteric developed. Ethylene did not overcome inhibition of ripening by cycloheximide. The respiratory climacteric is not inhibited by cycloheximide. It is concluded that normal ripening of pome fruits is a highly coordinated process of biochemical differentiation involving directed protein synthesis.

Journal Article↗

PubMedDate not supplied

Penetration of fosfomycin into cerebrospinal fluid across non-inflamed and inflamed meninges.

Serum and cerebrospinal fluid (CSF) concentrations of fosfomycin were evaluated in 45 patients. Mean serum concentration was 260.1 mg/l at 15 min postinfusion in 35 patients receiving a 5 g bolus dose, and 440 mg/l in five patients receiving a 10 g bolus dose. Mean distribution volume was 18.5 l (5 g dose), the total clearance was 118.8 ml/min, half-life was nearly 2 h, and the determined AUC were 420.95 mg/l.h (5 g dose) and 423.57 mg/l.h (10 g dose). The average peaks at 360 min in CSF reached 11.6 mg/l (5 g dose) and 17.7 mg/l (10 g dose). The CSF/serum ratio was 9.24% (5 g dose), and 13.81% (10 g dose). The CSF levels were not below 30 mg/l from the second day on in patients receiving 3 X 5 g fosfomycin per day. Meningeal inflammation increased the CSF concentrations from 30 mg/l at 6 h up to 150 mg/l at 120 h in the saturation phase, e. g., up to 300% more in comparison to non-inflamed meninges.

Adolescent↗