Search PubMed⌕ Search

Biomedical subjects

S N Chatterjee

Publications and source records attributed to S N Chatterjee.

At least 37 records · Page 2Linked to original sources
PubMed1994

UVA-induced peroxidation of lipid in the dried film state.

Exposure of a dried lipid thin film to UVA produced a dose-dependent linear increase in the three peroxidation products, conjugated diene, lipid hydroperoxide and malondialdehyde (MDA). All three lipid peroxidation products exhibited an inverse dose rate effect. Identical amounts of malondialdehyde were produced when the lipid film was exposed to UVA either directly or through the thickness of the Corning glass on which the film was cast. Antioxidants, alpha-tocopherol, butylated hydroxytoluene (BHT) and the singlet oxygen quencher beta-carotene significantly inhibited the UVA-induced peroxidation of the lipid film. The biological implications of the UVA-induced peroxidation of the dried lipid film are discussed.

Antioxidants↗
PubMed1994

Effect of rehydrating fluid 'Electral' on Vibrio cholerae cells.

V. cholerae OGAWA 154 cells underwent rapid loss of colony forming capacity during the first few minutes' incubation in the Electral medium at 37 degrees C, the turbidity of the suspension however increasing with time of incubation and leading to a plateau from 5 min onward. The vibrio suspension in the Electral medium released small amounts of 280 nm and much higher amounts of 260 nm absorbing materials. On withdrawal of the Electral medium, the cells underwent significant liquid holding recovery in the phosphate buffered saline, pH 7. Majority of the cells underwent no significant ultrastructural change but grew into long filamentous forms. The mode of action of the Electral medium on the vibrios is discussed.

Rehydration Solutions↗
PubMed1993

Induction of SOS like responses by nitrofurantoin in Vibrio cholerae el tor cells.

Treatment of Vibrio cholerae el tor strain SLH22(J) with nitrofurantoin induced dose-dependent prophage 'kappa', the maximum induction being 6-fold the spontaneous induction level. UV-inactivated 'kappa' phages were Weigle reactivated, the maximum Weigle factor being 1.8 and 2.0 respectively in nitrofurantoin and UV pretreated el tor strain H218 Smr. Nitrofurantoin treatment also caused significant filamentation of the el tor strain H218 Smr and mutation of these cells from ampicillin sensitivity to ampicillin resistance. The levels of the four SOS-like responses induced by this drug were low but significant.

Bacteriophages↗
PubMed1993

Electron microscopic study of phages and aberrant structures produced by induction of prophage kappa in Vibrio cholerae el tor cells.

Prophage kappa in V. cholerae el tor strain SLH22(J) could be induced spontaneously or by treatment with nitrofurantoin, though the efficiency of induction was very low (not more than 0.8%). V. cholerae el tor cells were found to release many different aberrant structures of the temperate phage, kappa. These aberrant structures were characterized by density gradient centrifugation and electron microscopy.

Bacteriophages↗
PubMed1993

Effects of nitrofurantoin on viability, DNA synthesis and morphology of Vibrio cholerae cells.

Nitrofurantoin caused a dose dependent inhibition of growth and decrease in viability of V. cholerae cells, the 10% (D10) and 37% (D37) survival doses being 50 and 19 micrograms/ml respectively. The drug at a concentration of 60 micrograms/ml caused 86% inhibition of DNA synthesis. Both light and electron microscopic observations revealed that treatment with nitrofurantoin (60 micrograms/ml for 1 hr at 37 degrees C) led to a significant filamentation of the V. cholerae cells, ultrastructure of the cell cytoplasm, plasma membrane and cell wall however remaining unaltered from those of untreated cells. The results are discussed in relation to DNA lesions produced by and the carcinogenic potential of the drug.

Cell Division↗
PubMed1993

Effect of UV-A on the linolenic acid micelles.

UV-A produced a dose-dependent linear increase of peroxidation in linolenic acid micelles as detected by the assay of (i) conjugated dienes, (ii) hydroperoxides, (iii) malondialdehyde (MDA), and (iv) the fluorescent adduct formed by the reaction of MDA with the amino acid, glycine. While sodium formate, dimethyl sulfoxide, superoxide dismutase, and ethylenediamine-tetraacetic acid produced no significant inhibition, some generally used singlet oxygen quenchers, beta-carotene, dimethylfuran, L-histidine, and sodium azide, caused significant inhibition of the UV-A-induced peroxidation of the linolenic acid micelles. alpha-Tocopherol and butylated hydroxytoluene produced more than 90% inhibition of the UV-A-induced peroxidation. ESR spectrometry revealed the formation of 2,2,6,6-tetramethylpiperidine oxide in the UV-A-irradiated aqueous solution of 2,2,6,6-tetramethylpiperidine. The involvement of singlet oxygen (1O2) in the UV-A-induced peroxidation of linolenic acid micelles is discussed.

Dose-Response Relationship, Radiation↗
PubMed1993

Induction of prophage lambda by nitrofurantoin and its modulation by butylated hydroxytoluene, sodium arsenite and alpha tocopherol.

Nitrofurantoin induced prophage-lambda in E. coli K12 strain GY5027(lambda) in a dose dependent manner, the maximum induction being 10-fold the spontaneous induction level and the maximum efficiency of induction 74%. The lever extract used as a metabolizing mixture enhanced the induction level significantly. Chloramphenicol at a concentration of 20 micrograms/ml inhibited the prophage induction by nitrofurantoin, indicating that the induction required concomitant protein synthesis. Butylated hydroxytoluene(BHT) and sodium arsenite enhanced the nitrofurantoin induced prophage-lambda induction in E. coli GY 5027(lambda) cells in a dose dependent manner. The maximum modulations in induction level (I/Io) were achieved with 100 micrograms/ml BHT and 250 micrograms/ml sodium arsenite corresponding to a nitrofurantoin concentration of 15 micrograms/ml and were found significant on statistical analysis. alpha-tocopherol, however, did not produce any effect on the prophage-lambda induction by nitrofurantoin.

Arsenic↗
PubMed1992

Adaptive response of Vibrio cholerae and Escherichia coli to nitrofurantoin.

Pretreatment with sublethal doses of nitrofurantoin induced adaptive response in both Vibrio cholerae and Escherichia coli cells as indicated by their greater resistance to the subsequent challenging doses of the same drug. Adaptive response was maximum corresponding to pretreatment drug concentrations of 0.40 microgram/ml and 0.015 microgram/ml respectively for V. cholerae OGAWA 154 (wild type) and E. coli K-12 AB 2463 (recA-) cells. Adaptive response was inhibited by chloramphenicol (100 micrograms/ml) indicating the need of concomitant protein synthesis. Induction of adaptive response in recA deficient E. coli cells indicated that it was different from the conventional "SOS" response. Melting temperature of DNA of V. cholerae cells subjected to adaptive (0.4 microgram/ml for 1 hr) and challenging (120 micrograms/ml for 1 hr) doses of nitrofurantoin (76 degrees C) was closer to that of native DNA (75 degrees C) vis-a-vis DNA isolated from nonadapted and drug treated cells (77.5 degrees C). Also, DNA isolated from V. cholerae cells subjected to adaptive and challenging doses of the drug revealed the presence of fewer interstrand cross-links (16% reversible DNA) vis-a-vis DNA from nonadapted but drug treated cells (55% reversible DNA). Photomicrographic studies revealed that V. cholerae cells that were nonadapted but drug treated grew into long filamentous forms (4.25 +/- 2.97 micron) whereas those subjected to both adaptive and challenge doses of the drug exhibited much less filamentation (2.08 +/- 0.84 micron) vis-a-vis native cells (1.42 +/- 0.5 micron). Similar results on DNA melting temperature, cross-links in DNA, and filamentation of cells were obtained for E. coli AB 2463 (recA-) cells subjected to adaptive and challenging treatments with nitrofurantoin. Almost equal degree of resistance against nitrofurantoin could be induced in both V. cholerae OGAWA 154 (wild type) and E. coli strain PJ3 (AB 1157 ada-) when these cells were pretreated with nontoxic doses of hydrogen peroxide or nitrofurantoin. Evidence obtained in this work on the nature of the nitrofuratoin induced adaptive response with particular references to the oxidative and/or alkylating DNA damages were discussed. Nitrofuratoin induced adaptive response appeared similar to that elicited by furazolidone in V. cholerae cells and appeared to be directed towards oxidative and not alkylating adaptive repair pathway.

Adaptation, Physiological↗
PubMed1992

In-vitro interaction between nitrofurantoin and Vibrio cholerae DNA.

In-vitro interaction of nitrofurantoin with V. cholerae DNA resulted in a quenching and red spectral shift of the drug absorption pattern. Scatchard analysis revealed that the drug binding involved more than one processes and that the strongest mode of binding was characterised by an association constant (k) of 5.04 x 10(6) M-1 and the number of binding sites per nucleotide (n) of 0.015. Based on viscosity measurements, the mode of drug binding to DNA appeared to be through intercalation, the helix unwinding angle of supercoiled plasmid pBR322 DNA being 10 degrees. Nitrofurantoin binding to DNA resulted in an elevation of the thermal melting temperature (Tm) of DNA by 6 degrees C and inhibition of the action of DNase on DNA.

Binding Sites↗
PubMed1992

On the induction of umu gene expression in Salmonella typhimurium strain TA1535/pSK1002 by some nitrofurans.

Several nitrofurans were found to induce umu gene expression in Salmonella typhimurium TA1535/pSK1002 as defined on the basis of at least a 2-fold increase of beta-galactosidase activity over the background level. beta-Galactosidase activity increased with increasing concentrations of the chemical, attained a maximum at a concentration which was different for different nitrofurans used, and then gradually decreased with a further increase of the nitrofuran concentration. The umu gene expression test revealed that the genotoxic activity was highest for furazolidone and lowest for 5-nitro-2-furaldehyde.

Azides↗
PubMed1991

X-ray inactivation, Weigle reactivation, and Weigle mutagenesis of the lysogenic Vibrio kappa phage.

Vibrio cholerae lysogenic kappa phage was inactivated by X-ray (60 kV) in a dose-dependent manner, the inactivation dose leading to 37% survival (D37) in phosphate-buffered saline (PBS), pH 7.4, being 0.36 kGy. The phages were significantly protected against X-ray irradiation when histidine or cysteine or both were present in PBS or when phages were irradiated in nutrient broth. Maximum protection was offered when both histidine (10.0 mM) and cysteine (10.0 mM) were present in PBS (dose enhancement factor being 4.17). The X-irradiated kappa phages also underwent a small but significant Weigle reactivation and also Weigle mutagenesis in the UV-irradiated V. cholerae host H218Smr. The Weigle factor or the frequency of clear-plaque mutants increased with increasing UV dose, attained a maximum at a UV dose of 2.4 J m-2, and thereafter decreased gradually with a further increase of the UV dose. The X-ray dose (D)--survival (S) curves could be empirically described by the equation S = exp[-(aD + bD2)], where a and b are constants depending on the irradiation conditions, and a good agreement between the theoretical curves and experimental data was obtained.

Bacteriophages↗
PubMed1990

DNA damage and prophage induction and toxicity of nitrofurantoin in Escherichia coli and Vibrio cholerae cells.

Repair-deficient and repair-proficient strains of E. coli K12 were sensitive to nitrofurantoin treatment to varying degrees with the double mutant strain (uvrA 6, recA 13) being most sensitive. Ultraviolet absorption data and thermal chromatography through a hydroxyapatite column revealed that nitrofurantoin treatment of V. cholerae strain OGAWA 154 produced a maximal amount of 55% reversibly bihelical DNA at a nitrofurantoin dose of 120 micrograms/ml/h, which indicated the formation of inter-strand cross-links in DNA. Nitrofurantoin also produced prophage-lambda induction in E. coli K12 strain GY 5027: envA, uvrB, ampA 1, strA (lambda), in a dose-dependent manner, the maximum induction being highly significant (P less than 0.001). Previously published mutation data coupled with the prophage induction data presented here suggest that the genotoxic properties of nitrofurantoin are mediated through the SOS pathway.

Bacteriophage lambda↗
PubMed1990

DNA damage and cell killing by nitrofurantoin in relation to its carcinogenic potential.

Nitrofurantoin inhibited growth and produced loss of viability of Vibrio cholerae cells in a dose-dependent manner, the 10% (D10) and 37% (D37) survival doses being 18.0 and 5.5 micrograms/ml x hr. respectively. The drug also caused filamentation of the cells in a very significant manner. Ultraviolet absorption data and thermal chromatography through hydroxyapatite column revealed that nitrofurantoin treatment of Vibrio cholerae cells produced a maximum amount of 55% of DNA reversibly bihelical due to the formation of inter-strand cross-links. Helix-coil transition studies carried out by viscometric and also, spectrophotometric methods revealed that the nitrofurantoin-induced cross-links in Vibrio cholerae DNA, imparted to this DNA greater thermal stability than that of native DNA. The quantitative aspect and also the mode of nitrofurantoin action on DNA of Vibrio cholerae and Escherichia coli cells vis-à-vis the carcinogenic potential of the drug were discussed.

Carcinogens↗
PubMed1990

The induction of lipid peroxidation in liposomal membrane by ultrasound and the role of hydroxyl radicals.

Ultrasonic radiation produced a dose-dependent linear increase in lipid peroxidation in the liposomal membrane as reflected in the measurements of conjugated dienes, lipid hydroperoxides, and malondialdehydes (MDA). Production of MDA was confirmed by spectrophotometric and spectrofluorometric methods including the detection of excitation (360 nm) and emission (435 nm) maxima characteristic of the MDA-glycine adduct formed after addition of glycine in the system. Ultrasound of frequencies 20 kHz (used for laboratory purposes) and 3.5 MHz (used for clinical purposes) produced MDA in an identical manner. Ultrasound-induced lipid peroxidation was enhanced synergistically by 2.5 X 10(2) microM ascorbic acid but inhibited significantly by 10(4) microM ascorbic acid. Ultrasound-induced production of MDA could not be inhibited to any significant degree by superoxide dismutase, histidine, dimethylfuran, or beta-carotene but was very significantly inhibited by cholesterol (93%), butylated hydroxytoluene (88%), alpha-tocopherol (85%), sodium benzoate (80%), dimethyl sulfoxide (80%), sodium formate (64%), and EDTA (64%). The scavenger studies indicated the functional role of OH radicals in the initiation of ultrasound-induced lipid peroxidation.

Hydroxides↗
PubMed1990

An approach towards understanding the genesis of sunlight-induced skin cancer.

The molecular basis of the sunlight-induced skin carcinogenesis has been elucidated. Of the two ultraviolet components of sunlight that reach the earth's surface the UV-B is known to be carcinogenic but the mode of action of UV-A, the predominant component of sunlight, is ill understood. Using the liposomes as a model system, it has been shown here that UV-A causes dose-dependent lipid peroxidation as estimated by measurements of conjugated dienes, lipid hydroperoxides, malondialdehydes and the fluorescent adducts (Schiff bases) produced by the reaction of MDA with glycine. Direct exposure to sunlight has also been shown to cause dose-dependent lipid peroxidation. The UV-A induced lipid peroxidation has also been shown to be dependent on dose rate. While the sodium formate, dimethyl sulphoxide, superoxide dismutase and EDTA do not have any significant effect, sodium azide, histidine, beta-carotene and dimethylfuran were shown to inhibit significantly the UV-A induced lipid peroxidation, thereby providing significant evidence of the involvement of singlet oxygen (1O2) as the initiating agent. The use of D2O in place of H2O as the liposome dispersing medium enhanced to great extent the UV-A induced lipid peroxidation, thereby lending additional support to the finding that singlet oxygen was the initiating agent. The possible mode of formation of 1O2 on exposure to UV-A was discussed. This study also highlighted the role of environmental factors on the sunlight-induced cutaneous damage. Finally, the relation between lipid peroxidation, DNA damage and carcinogenesis has been discussed in a way to suggest the possible link between sunlight exposure and causation of skin cancer.

Humans↗
PubMed1990

Membrane lipid peroxidation by UV-A: mechanism and implications.

UV-A produced a dose-dependent linear increase of lipid peroxidation in liposomal membrane, as detected by the assay of (i) conjugated dienes, (ii) lipid hydroperoxides, (iii) malondialdehydes (MDA), and (iv) the fluorescent adducts formed by the reaction of MDA with glycine and also a linear dose-dependent increase of [14C]glucose efflux from the liposomes. UV-A-induced MDA production could not be inhibited by any significant degree by sodium formate, dimethyl sulfoxide, EDTA, or superoxide dismutase but was very significantly inhibited by butylated hydroxytoluene, alpha-tocopherol, sodium azide, L-histidine, dimethylfuran, and beta-carotene. MDA formation increased with an increase in the D2O content in water, leading to a maximal amount of nearly 50% enhancement of lipid peroxidation in 100% D2O vis-à-vis water used as dispersion medium. The experimental findings indicate the involvement of singlet oxygen as the initiator of the UV-A-induced lipid peroxidation.

Antioxidants↗
PubMed1989

UV-A induced lipid peroxidation in liposomal membrane.

UV-A (365 nm) produced a dose-dependent linear increase of lipid peroxidation, as detected by the assay of malondialdehyde (MDA). MDA formation was inversely related to the UV-A dose rate. Sodium formate and ethylenediaminetetra acetic acid (EDTA) could not inhibit by any significant degree the UV-A induced MDA formation. While butylated hydroxy toluene (BHT) caused about 85% inhibition, sodium azide and L-histidine produced 45-50% inhibition of MDA formation. The involvement of singlet oxygen (1O2) in the UV-A induced lipid peroxidation is discussed.

Free Radicals↗