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Biomedical subjects

B M Mehta

Publications and source records attributed to B M Mehta.

48 records · Page 3Linked to original sources
PubMed1973

Effects of energy metabolism on the release of bound proflavine from sensitive and resistant Escherichia coli.

Proflavine inhibited the aerobic and anaerobic utilization of glucose by sensitive but not by resistant Escherichia coli. In resistant cells that had bound proflavine, glucose utilization was accompanied by release of the dye. After glucose was used up, the cells could again take up proflavine. If the amount of proflavine bound to sensitive cells was too low to inhibit glucose utilization, adding glucose to these cells caused them to release the dye. With higher proflavine concentrations, inhibitory to glucose utilization, the dye remained cell bound. Thus, metabolic energy causes the release of proflavine by both sensitive and resistant cells. In the former, energy production is inhibited by proflavine, and thus the dye prevents its own release. Chloramphenicol did not interfere with metabolically induced release of proflavine from resistant cells. Cyanide inhibited the glycerol-induced loss of proflavine, but not the glucose-induced loss. Azide and carbonyl cyanide m-chlorophenylhydrazone could prevent proflavine release without inhibiting glucose utilization.

Acridines↗
PubMed1972

The elusive permeability barriers and binding sites for proflavine in Escherichia coli.

Cells of proflavine-sensitive and -resistant Escherichia coli strains were altered in different ways, and the proflavine binding of the changed material was studied. Spheroplasts prepared from sensitive and resistant cells bound similar amounts of proflavine at saturation, whether or not they were osmotically protected by 10% sucrose. Intact cells bound approximately the same amounts of proflavine as spheroplasts. On addition of glucose, osmotically protected resistant but not sensitive spheroplasts released proflavine; unprotected spheroplasts did not release bound proflavine. Thus, osmotically protected membranes are not required for proflavine binding (a passive process) but are required for proflavine release (an active process). The presence of sucrose reduced proflavine binding by resistant cells. Adding glucose to cells in 20% sucrose did not cause a release of residual proflavine, though glucose caused a release of proflavine from cells suspended in 0 or 10% sucrose. On treatment of heated cells or ruptured spheroplasts with nucleases and Pronase, practically all nucleic acids were removed. Proflavine-binding ability of such preparations fell by only 30 to 50%. Washing heated cells with ethanol did not reduce their proflavine-binding ability. There appear to be important binding sites in cells aside from nucleic acids.

Acridines↗
PubMedDate not supplied

Reversibility of elemental liquid diet-enhanced methotrexate toxicity by refeeding with chow.

The toxic effects of methotrexate administration [20 mg/kg, bolus intraperitoneally (ip)] to rats fed a regular chow diet (n = 10) was compared with results in animals fed an elemental, chemically defined, liquid diet (n = 10) for 7 days. All animals receiving an elemental diet became anorectic and lethargic within 60 hr of methotrexate injection. All animals in this group subsequently developed enteritis and died within 150 hr. There was no clinical evidence of enteritis in rats fed a regular chow diet and mortality as zero in this group (p less than 0.001). In a second study one group of rats (n = 9) was fed a regular chow diet for 7 days; four groups were fed an elemental, chemically defined, liquid diet (n = 9 per group) for 7 days. At 24 hr and 8 hr prior to, or 24 hr after methotrexate administration, one group was refed a regular chow diet; the fourth group was maintained on an elemental liquid diet throughout the study period. All rats fed a regular chow diet survived following methotrexate injection (20 mg/kg, ip). All rats fed an elemental diet throughout the study period died. Those rats refed a regular diet 24 or 8 hr prior to methotrexate injection demonstrated a significant improvement in survival (100% in the 24-hr group, 55% in the 8-hr group). However, those animals refed a regular diet 24 hr after methotrexate injection demonstrated a 100% mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Assay for citrovorum factor (NSC-3590) in the presence of methotrexate (NSC-740).

Treatment of certain malignancies with high-dose methotrexate/citrovorum factor rescue has recently been adopted as an effective regimen. A microbiologic assay capable of detecting citrovorum factor in the presence of massive amounts of methotrexate has been developed using a strain of Pediococcus cerevisiae resistant to methotrexate. The assay described in this paper is an inexpensive and rapid method of studying the distribution kinetics of citrovorum factor.

Adult↗
PubMedDate not supplied

Microbiologic assay for cytosine arabinoside (NSC-63878): the use of a mutant of streptococcus faecium var. durans resistant to methotrexate (NSC-740) and 6-mercaptopurine (NSC-755).

Cytosine arabinoside has been shown to be effective in the treatment of acute leukemias and lymphomas, especially in combination with other established anticancer agents such as methotrexate, 6-mercaptopurine, and 6-thioguanine. A microbiologic assay capable of detecting cytosine arabinoside in the presence of such anticancer agents in body fluids has been developed using a strain of Streptococcus faecium var. durans resistant to methotrexate and 6-mercaptopurine; the assay can also be used to determine cytosine arabinoside concentrations in the presence of l-thioguanine. In view of the present trend toward drug combinations, including those using tetrahydrouridine, in the chemotherapy for human neoplasms, the proposed assay method will be valuable in cytosine arabinoside distribution studies.

Biological Assay↗