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Biomedical subjects

G Cohen

Publications and source records attributed to G Cohen.

At least 505 records · Page 28Linked to original sources
PubMed1969

Catalase-aminotriazole method for measuring secretion of hydrogen peroxide by microorganisms.

A new method for measuring the secretion of H(2)O(2) has been based upon an H(2)O(2)-dependent inhibition of catalase by 3-amino-1,2,4-triazole. The conversion of an H(2)O(2)-secretion rate into a catalase inhibition rate amplified a relatively small molar concentration of H(2)O(2) and provided a highly specific and sensitive method for quantitatively measuring H(2)O(2). A major advantage of this approach is that it does not require extensive accumulation of H(2)O(2) in the environment. The method was successfully employed to measure H(2)O(2) secretion by Mycoplasma pneumoniae, which possesses a peroxidase-like activity that limits the accumulation of H(2)O(2) in the environment.

Bacteria↗
PubMed1969

Glucose-dependent secretion and destruction of hydrogen peroxide by Mycoplasma pneumoniae.

The secretion of H(2)O(2) by Mycoplasma pneumoniae and M. gallisepticum was measured with the new catalase-aminotriazole method. Peroxide secretion by the mycoplasmas was stimulated by glucose. When catalase and aminotriazole were omitted and exogenous H(2)O(2) was added to the mycoplasmas, a loss in H(2)O(2) was noted with time; the addition of glucose speeded the disappearance of H(2)O(2). The presence of this peroxidase-like activity in the mycoplasmas explains an observed failure of H(2)O(2) to accumulate freely in the suspension medium.

Catalase↗
PubMed1967

Peroxidative hemolysis of red blood cells from patients with abetalipoproteinemia (acanthocytosis).

The effect of peroxidative stress on tissue was studied by exposure of red blood cells (RBC) from patients with abetalipoproteinemia to minute amounts of H(2)O(2)in vitro. Red blood cells from untreated patients showed a marked sensitivity to H(2)O(2), as evidenced by hemolysis and lipid peroxidation (peroxidative hemolysis). The appearance of lipid peroxidation products in sensitive cells after exposure to H(2)O(2) was indicated by 1) increases in the 2-thiobarbituric acid (TBA) reaction of trichloroacetic acid extracts, 2) increases in ultraviolet light absorbency of lipid extracts, and 3) decreases in polyunsaturated fatty acids. These changes were accompanied by a decrease in phosphatidyl ethanolamine and phosphatidyl serine in the RBC lipid extract. Similar lipid changes on exposure to H(2)O(2) were observed in the RBC from vitamin E-deficient rats. Treatment of the patients with d-alpha-tocopherol polyethylene glycol succinate by mouth, or addition of dl-alpha-tocopherol to the incubation medium protected the RBC from peroxidative hemolysis. Tocopherol appears to provide a primary biologic defense against peroxidative hemolysis. The presence of nitrite or carbon monoxide, which produced methemoglobin and carboxyhemoglobin, respectively, inhibited peroxidative changes, suggesting a catalytic role for oxy- or deoxyhemoglobin. Substances that prevented lipid peroxidation also prevented hemolysis; in addition, lipid peroxidation appeared to precede hemolysis. These observations suggested that hemolysis was a consequence of lipid peroxidation.

Abetalipoproteinemia↗
PubMedDate not supplied

Lipid peroxidation: detection in vivo and in vitro through the formation of saturated hydrocarbon gases.

Saturated, short-chain hydrocarbon gases (ethane, propane, etc.--but not methane) are evolved during the spontaneous lipid peroxidation of mouse tissue slices or homogenates. A relatively-selective increase in either ethane or pentane was observed when either linolenic acid or linoleic acid, respectively, was added to tissue homogenates. When mice were challenged by injection of carbon tetrachloride or cumene hydroperoxide (two agents that induce a lipid peroxidative attack on liver), they exhaled ethane. The gas chromatographic detection and monitoring of hydrocarbon gases can serve as an index of lipid peroxidation in vivo.

Animals↗
PubMedDate not supplied

Protection and inflammatory markers following exposure of guinea pigs to sarin vapour: comparative efficacy of three oximes.

The purpose of the present study was to compare the antidotal efficacy and the combined effects on inflammatory markers of three oximes--toxogonine, TMB4 and 2-PAM--in combination with anticholinergic drugs following exposure to sarin vapour by inhalation. Guinea pigs restrained in plethysmographs were exposed to various doses of sarin vapour (in the range of 1.4-4.4LD50). The antidotal mixture was injected immediately (5-20 s) following exposure (3 mg kg(-1) atropine and 1 mg kg(-1) benactyzine in combination with 6 mg kg(-1) toxogonine, 2 mg kg(-1) TMB4 or 12 mg kg(-1) 2-PAM). Bronchoalveolar lavage (BAL) samples were taken from surviving animals 24 h after exposure to determine the levels of inflammatory markers. A differential cell count was performed in BAL samples on Giemsa-stained slides. The inflammatory markers--histamine and prostaglandins (PGE)--were measured in BAL using radioimmunoassay (RIA) techniques. The survival rate in the various treatment groups and analysis of BAL samples showed that: (i) Toxogonine, TMB4 and 2-PAM, without pyridostigmine pretreatment, at doses that were proportional to their doses in the respective auto-injectors, exhibited similar antidotal efficacy against sarin exposure. (ii) The results demonstrated that a centrally acting anticholinergic drug is essential in the antidotal mixture to ensure survival. (iii) Histamine release and eosinophilia following sarin inhalation might require additional intervention, aimed at reducing the symptoms of allergic reaction and possibly expediting recovery.

Animals↗