Biomedical subjects
Publications and source records attributed to E H Marth.
During lactation, 5 female mink (Mustela vison) were given 50 mug of aflatoxin B1 orally twice, 2 weeks apart. Another group of 5 lactating mink were used as controls, Milk was collected 24 hours after each treatment with toxin. Aflatoxin B1 and M1 could not be detected in the milk. There was no appreciable difference in body weight among kits that nursed treated mink and those that nursed untreated mink.
Aflatoxins B1, B2, G1, and G2 were degraded by the 8- and 16-day old but not by the 4-day old mycelium of a toxigenic strain of Aspergillus parasiticus. The 16-day old mycelium degraded the toxin more rapidly than did the 8-day old mycelium. Degradation of toxin by the mycelium was similar at pH 2.5 and 6.0.
Spores of an aflatoxigenic strain of Aspergillus parasiticus were inoculated into a glucose-salts medium which was incubated with and without shaking at 28 degrees C for 15 days. Without shaking, maximal production of total aflatoxin and aflatoxins B1, G1, and G2 occurred at 5 days, whereas the maximal amount of B2 appeared after 7 days. Initially approximately 5% of the total toxins appeared in the mycelium but this increased to more than 60% after 5 days. Shaking of cultures during incubation served to reduce production of total aflatoxin and of each of the individual toxins. The maximal amount of total aflatoxin and of toxins B1 and G1 appeared in shaken cultures after 5 days, whereas 8 and 11 days were needed to obtain maximal amounts of B2 and G2, respectively. The mycelium of shaken cultures initially retained approximately 50% of the total aflatoxin and this increased to about 80% as the incubation progressed. Very little aflatoxin was synthesized at 35 and 45 degrees C and production of total aflatoxin and of each individual toxin was less at 15 degrees C than at 25 or 28 degrees C. When the medium contained 0.5 to 50% glucose, maximal amounts of total aflatoxin and of aflatoxins B1, G1 and G2 appeared in the presence of 30% glucose; only 20% glucose was needed to obtain the greatest amount of B2. The mycelium retained approximately 50% of total aflatoxin when the medium contained 5 to 20%. Neither aflatoxin G1 nor G2 were detected when the medium contained 0.05% ammonium sulfate and only B1, B2, and G1 appeared in the medium with 0.1% of the salt. Maximal production of each individual aflatoxin and of total aflatoxin occured with 1% of ammonium sulfate in the medium. The proportion of total aflatoxin retained by the mycelium decreased from 83 to 37% as the amount of ammonium sulfate in the medium was increased from 0,05 to 10%.
Saccharomyces cerevisiae was incubated in aerosol cans containing YM broth and dichlorofluoromethane (f-21). The presence and number of viable cells were determined by inoculating (1% vol/vol) YM broth and by the plate count procedure (YM agar). Inactivation of the yeast was greater or more rapid when: (i) the thermodynamic activity (saturation value) of f-21 became greater through increasing the concentration of chemical from 0.5 to 1.5% (wt/wt) in a given volume (20, 40, or 80 ml) of broth, or by holding the concentration of chemical constant but increasing the volume of broth in the test vessel, (ii) the temperature of treatment was increased (7, 22, 37, and 47 C), (iii) samples with 1.5% (wt/wt) f-21 were agitated, (iv) young (8 h) rather than old (36 h or 10 days) cells were treated, and (v) cells were grown in YM broth without, rather than with, glucose. Adjusting the pH (6.3 to 4.0) of broth before treatment, pretreating the substrate with f-21, or distilling the chemical before use had no effect on viability of cells when treated with f-21. Yeast cells inactivated by f-21, chlorine, or heat were more resistant to disruption by sonic treatment than were viable cells.
Cells of Escherichia coli ML30 in a mineral salts medium were exposed to dichlorodifluoromethane (f-12), cyclopropane, halothane, or Ethrane at concentrations of 1.25, 0.2, 0.04, and 0.008 X saturation for times up to 1,200 min, and at temperatures in the range of 2 to 37 C. When any of these anesthetics were applied for 300 min at 1.25 X saturation, a substantial decrease in number of survivors occurred. Halothane was most bactericidal, cyclopropane and Ethrane were moderately bactericidal, and t-12 was least bactericidal. At saturation values of less than 1.0, none of the four anesthetics had an appreciable effect on viability of E. coli. Greatest increases in cell permeability occurred when anesthetics were used at saturation values of 1.25, and permeability changes generally decreased as the concentrations of the chemicals were reduced. In many instances, anesthetics in the vapor state caused significant increases in cell permeability but little or no loss of viability. This indicated that a close relationship did not exist between loss of viability and increased permeability. All four anesthetics caused E. coli to lose substantial and similar amounts of compounds absorbing at 260 nm. Release of compounds absorbing at 260 nm generally increased as the saturation value of a given chemical was increased. Halothane, Ethrane, and cyclopropane but not f-12 caused lysis of E. coli ML300. Considering all results, E. coli ML30 was damaged more by halothane or cyclopropane than by f-12 or Ethrane. When f-12 was applied at a saturation value of 1.25, the bactericidal effect on E. coli was much greater at 37 or 22 C than at 12 or 2 C.
The in vitro and in vivo incorporation of (2-14C)acetate into lipids of mink (Mustela vison) liver and intestines was studied. In vitro, a dose of aflatoxin B1 as small as 7.5 mug/ml of medium reduced by 20% the amount of (2-14C)acetate incorporated into lipids of mink liver slices, whereas 180 mug caused 76% reduction in the synthesis of lipids from the radioactive precusor. Similar inhibition of lipid synthesis by aflatoxin also was observed with tissues from mink intestines and fatty liver. The degree of inhibition (19 to 84% for tissue from intestines and 19 to 64% for tissue from fatty livers) depended on the amount of aflatoxin B1 (7.5 TO 180 MUG) present in the medium. In vivo, a substantially increased amount of 14C-labeled lipids was found in the livers of mink injected with 600 mug of aflatoxin B1 per kg of body weight 20, 28, and 40 h earlier. However, no appreciable difference in incorporation of (2-14C)acetate into lipids was observed between toxin-treated and control animals when these animals were sacrificed and examined for 14C-labeled lipids at 4 and 10 h after toxin was administered.
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Synthesis of total lipid and aflatoxin by Aspergillus parasiticus as affected by various concentrations of glucose and nitrogen in a defined medium and by different incubation temperatures was studied. Maximal yields of lipid and aflatoxin were obtained with 30% glucose, whereas mold growth, expressed as dry weight, was maximal when the medium contained 10% glucose. Maximal mold growth occurred when the medium contained 3% (NH(4))(2)SO(4); however, 1% (NH(4))(2)SO(4) favored maximum accumulation of lipid and aflatoxin. Growth of mold and synthesis of lipid and toxin also varied with the incubation temperature. Maximal mold growth occurred at 35 C, whereas most toxin appeared at 25 C. Maximal production of lipid occurred at 25 and 35 C but production was more rapid at 35 C. Essentially all glucose in the medium (5% initially) was utilized in 3 days at 25 and 35 C but not in 7 days at 15 and 45 C. Patterns for formation of lipid and aflatoxin were similar at 15 and 25 C when a complete growth medium was used and at 28 C when the substrate contained various concentrations of glucose or (NH(4))(2)SO(4). They were dissimilar when the mold grew at 35 or 45 C. At these temperatures lipid was produced preferentially and only small amounts of aflatoxin appeared.
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Up to approximately 50 mug of staphylococcal enterotoxin A per plate was produced by cellophane-over-agar cultures. Enterotoxin was determined by a latex agglutination technique.
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VARIOUS BACTERIA, YEASTS, AND MOLDS IMPORTANT TO THE FOOD INDUSTRY WERE INCUBATED IN AEROSOL CANS CONTAINING A C BROTH AND ONE OF THE FOLLOWING THREE GAS HYDRATE FORMERS: propane, dichlorodifluoromethane (f-12), and 1,1-difluoro-1-chloroethane (f-142b). Most hydrate formers were tested at three concentrations: low (vapor state), intermediate (liquid state, low level), and high (liquid state, high level). Samples were continuously agitated for 48 hr at 21 +/- 3 C. Changes in numbers of microorganisms were determined by plate count. With hydrate formers in the vapor state, propane was more toxic to the microorganisms tested than either f-12 or f-142b. The most resistant organisms from these trials were then tested against f-12 or f-142b in the liquid state. Hydrate formers were far more toxic in the liquid state than in the vapor state. With the exception of sporulated cultures of Bacillus cereus, all microorganisms tested were greatly reduced in numbers when agitated for 48 hr at 21 C in the presence of f-12 or f-142b.
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Nine vats of stirred-curd granular cheddar cheese were made with whole milk contaminated with Salmonella typhimurium after pasteurization. Enumeration of salmonellae by the most probable number technique during manufacture and curing showed that these organisms multiplied rapidly during manufacture until the curd was salted. Thereafter and throughout the curing period, the salmonellae declined in number at a rate dependent on the temperature of curing. Evidence is presented indicating that the production of volatile fatty acids in the curd during curing may be responsible for this decline.
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