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At least 19 recordsLinked to original sources
PubMed1975

[Caffeine as an inhibitor of the conjugation transfer of R-factors. A study of certain aspects of the mechanism of action of caffeine on the conjugation transfer of R-factors].

Some aspects of the inhibitory effect of caffeine on conjugation transfer of R-factors described by the authors earlier were studied. The effect of the above substance on the donor and recipient competence was tested in experiments with cultivation of the parent strains for 18 hours in the presence of caffeine. For this purpose the effect of caffeine on reduction of the donor and recipient cell competence after starvation in a physiological solution was investigated. It was shown that caffeine markedly decreased the donor competence of strain 15-3Mdrd of E. coli in the experiments of both types. Caffeine also inhibited reduction of the recipient competence of strain C600 of E. coli after starvation without its changing on 18-hour treatment. For the study of the caffeine effect on formation of the conjugation pairs experiments were carried out with dilution of the conjugation mixture after definite intervals which practically stopped formation of new conjugation pairs and eliminated further effect of caffeine on conjugation. Under such conditions transfer of R-factors may occur in the conjugation pairs after elimination of caffeine by dilution, if they were formed in the presence of caffeine before the mixture dilution. The experiments showed that caffeine inhibited not the formation of the conjugation pairs but the genetic transfer of R-factors. In addition, it was found that the substance insignificantly inhibited the process of phenotypic manifestation of the resistance markers. Inhibition of conjugation R-transfer by caffeine was associated with its eliminating effect, since the concentrations used did not induce elimination of the resistance markers in R+ strains.

Caffeine↗
PubMed1976

Replicative bypass repair of ultraviolet damage to DNA of mammalian cells: caffeine sensitive and caffeine resistant mechanisms.

Replicative bypass repair of UV damage to DNA was studied in a wide variety of human, mouse and hamster cells in culture. Survival curve analysis revealed that in established cell lines (mouse L, Chinese hamster V79, HeLa S3 and SV40-transformed xeroderma pigmentosum (XP)), post-UV caffeine treatment potentiated cell killing by reducing the extrapolation number and mean lethal UV fluence (Do). In the Do reduction as the result of random inactivation by caffeine of sensitive repair there were marked clonal differences among such cell lines, V79 being most sensitive to caffeine potentiation. However, other diploid cell lines (normal human, excision-defective XP and Syrian hamster) exhibited no obvious reduction in Do by caffeine. In parallel, alkaline sucrose sedimentation results showed that the conversion of initially smaller segments of DNA synthesized after irradiation with 10 J/m2 to high-molecular-weight DNA was inhibited by caffeine in transformed XP cells, but not in the diploid human cell lines. Exceptionally, diploid XP variants had a retarded ability of bypass repair which was drastically prevented by caffeine, so that caffeine enhanced the lethal effect of UV. Neutral CsC1 study on the bypass repair mechanism by use of bromodeoxyuridine for DNA synthesis on damaged template suggests that the pyrimidine dimerer acts as a block to replication and subsequently it is circumvented presumably by a new process involving replicative bypassing following strand displacement, rather than by gap-filling de novo. This mechanism worked similarly in normal and XP cells, whether or not caffeine was present, indicating that excision of dimer is not always necessary. However, replicative bypassing become defective in XP variant and transformed XP cells when caffeine was present. It appears, therefore, that the replicative bypass repair process is either caffeine resistant or sensitive, depending on the cell type used, but not necessarily on the excision repair capability.

Caffeine↗
PubMed1975

Mitigation of caffeine-induced teratogenicity in mice by prior chronic caffeine ingestion.

Pregnant A/J female mice, which had drunk tap water or a 0.05% caffeine solution for 8-19 weeks after weaning, were each injected sc with 150 or 250 mg/kg caffeine once on day 13 of gestation. After 150 mg/kg caffeine the frequencies at term of fetal death, external malformation, and subcutaneous hematomas were significantly lower in the caffeine- than water-drinking group. After 250 mg/kg caffeine the frequency of fetal death but not of malformations and hematomas was lower in the group with caffeine pretreatment. These findings were explained by assuming that long-term ingestion of caffeine induced and increased rate of degradation of caffeine administered during pregnancy.

Abnormalities, Drug-Induced↗
PubMed1975

Biosynthesis of caffeine by tea-leaf extracts. Enzymic formation of theobromine from 7-methylxanthine and of caffeine from theobromine.

1. Extracts prepared from tea leaves with Polyclar AT (insoluble polyvinylpyrrolidine) contained two methyltransferase activities catalysing the transfer of methyl groups from S-adenosylmethionine to 7-methylxanthine, producing theobromine, and to theobromine, producing caffeine. 2. The methyltransferases exhibited the same pH optimum (8.4) and a similar pattern of effects by metal ions, thiol inhibitors and metal-chelating reagents, both for theobromine and caffeine synthesis. Mg2+, Mn2+ and Ca2+ slightly stimulated enzyme activity but they were not essential. Paraxanthine was shown to be most active among methylxanthines, as the methyl acceptor. However, the formation of paraxanthine from 1-methylxanthine was very low and that from 7-methylxanthine was nil, suggesting that the synthesis of caffeine from paraxanthine is of little importance in intact plants. Xanthine, xanthosine, XMP and hypoxanthine were all inactive as methyl acceptors, whereas [2(-14)C]xanthine and [8(-14)C]hypoxanthine were catabolized to allantoin and urea by tea-leaf extracts. The apparent Km values are as follows: 7-methylxanthine, 1.0 times 10(-14)M; theobromine, 1.0 times 10(-3)M; paraxanthine, 0.2 times 10(-3)M; S-adenosylmethionine, 0.25 times 10(-4)M (with each of the three substrates). 3. The results suggest that the pathway for caffeine biosynthesis is as follows: 7-methylxanthine leads to theobromine leads to caffeine. In contrast, it is suggested that theophylline is synthesized from 1-methylxanthine. The methyl groups of the purine ring of caffeine are all derived directly from the methyl group of S-adenosylmethionine. Little is known about the pathways leading to the formation of 7-methylxanthine. 4. A good correlation between caffeine synthesis and shoot formation or growth of tea seedlings was shown, suggesting that the methylating systems in caffeine synthesis are closely associated with purine nucleotide and nucleic acid metabolism in tea plants.

Caffeine↗
PubMed1975

[Caffeine as an inhibitor of the conjugation transfer of R-factors. A study of the quantitative effect of caffeine on the conjugation transfer of R-factors].

The effect of caffeine on the conjugation transfer of R-factors was studied using a standartized kinetic conjugation system described earlier. It was shown that caffeine had a pronounced inhibitory effect on R-factor transfer. The inhibition coefficients at a caffeine concentration of 2000 gamma/ml were from 2.5 (when using strain CSH-2 R222 of E. coli as the donor) to 13.8 (when using strain J5-3 RI drd of E. coli as the donor). Higher concentrations of caffeine induced a significant increase in the coefficient. Since R-transfer inhibition was induced by rather high concentrations of caffeine, the effect of equivalent concentrations of some normal metabolites of the purine and pyrimidine series, such as ATP, guanine, cytosine and thymine was studied. It was shown that the substances had no inhibitory effect on R-factor transfer. Inhibition of P-transfer by caffeine did not depend on either the type of R-factor or the microbial host.

Bacteriological Techniques↗
PubMed1978

Caffeine concentrations in mice plasma and testicular tissue and the effect of caffeine on the dominant lethal test.

Large groups of male Swiss mice received per os on average 100 mg caffeine per kg body weight per day for 1 or 8 weeks. The dominant lethal test was designed to achieve maximum sensitivity in order to detect any possible mutagenic effect. No mutagenic induction of dominant lethals, pre-implantation egg loss or depression of the fertility of females, caused by caffeine at the dose levels administered were observed. The half life of caffeine, which was between 2.5 and 3 h, was similar in plasma and testicular tissue. It was concluded that caffeine did not accumulate in the testicular tissue of mice. The maximum concentration of caffeine found was below 10 microgram/g testicular tissue, which is about a 100 times lower than concentrations that cause chromosome aberrations in cultured mammalian cells.

Animals↗
PubMed1979

Effects of caffeine on maternal repair systems in Drosophila melanogaster. Concentration-dependent reversals of the effects of caffeine on chromosome loss and autosome-autosome translocations induced by x-rays in the paternal genome.

Drosophila melanogaster females were treated with 1% caffeine, mated with X-rayed males and the frequencies of induced sex-chromosome loss, translocations between the major autosomes and between the Y-chromosome and the major autosomes determined. In a reversal of the results obtained previously with 0.2% caffeine by Mendelson and Sobels, treatment of females with 1% caffeine led to a decrease in sex-chromosome loss, confirming preliminary data of Zimmering and Osgood and an increase in autosome--autosome translocations. It is suggested that the higher concentration of caffeine inhibits replication permitting more time available for chromosome-type restitutions by means of caffeine-insensitive repair mechanisms. In contrast with results for autosome--autosome translocation, the frequency of Y-autosome translocations was depressed below controls suggesting an isolation (by any one of several means) of Y-chromosome breaks from those in the autosomes.

Animals↗
PubMed1975

Modification of the radiosensitivity of barley seed by post-treatment with caffeine. Kinetics of decay of caffeine-reactive oxygen-sensitive sites.

In dry barley seeds (3-1 per cent moisture content), the maximal level of oxic damage (class III damage) is reached within the first 40 min of post-hydration in oxygenated water at 5 +/- 1 degrees C. The decay of the gamma-ray-induced oxygen-sensitive sites requires, however, about 120 min. The mechanisms leading to partial protection against the class III damage are initiated when caffeine is present during the first 30 min of oxygenated post-hydration. If added after 30 min of oxygenated hydration, caffeine has no protective action. For the potentiation of an oxygen-independent component of damage, caffeine has to be present during the first 240 min of oxygen-free hydration. These observations involving a physiologically inert system raise questions regarding physico-chemical vis-a-vis biochemical mechanisms of caffeine effect on irradiated systems and these have been briefly discussed.

Caffeine↗
PubMed1978

A study of caffeine in tea. I. A new spectrophotometric micro-method. II. Concentration of caffeine in various strengths, brands, blends, and types of teas.

A new spectrophotometric micro-method for the determination of caffeine in tea is described. This method is then used to evaluate the caffeine content of a variety of brands and blends of bagged and loose hot tea prepared in different strengths and by different brewing methods. In addition, the caffeine content of instant tea, ice tea, and Mr. Coffee automatic tea is evaluated.

Caffeine↗
PubMed1992

Caffeine-derived N-nitroso compounds--I: Nitrosatable precursors from caffeine and their potential relevance in the etiology of oesophageal and gastric cancers in Kashmir, India.

Salted tea prepared in Kashmir by adding sodium bicarbonate shows high methylating activity (equivalent to 3 p.p.m. N-methylnitrosourea) upon in vitro nitrosation. Pure caffeine treated under conditions of the tea preparation formed caffeidine and caffeidine acid. We report here the formation of two new compounds, mononitrosocaffeidine, an asymmetric nitrosamine, and dinitrosocaffeidine, a N-nitrosamide, on in vitro nitrosation of caffeidine. Mononitrosocaffeidine is also found after nitrosation of the typical Kashmir tea. The nitrosation of caffeidine acid produced N,N'-dimethyl-parabanic acid, mononitrosocaffeidine and N,N'-dimethyl-N-nitrosourea. In view of the well-known structure-activity relationships of these N-nitroso compounds, their possible endogenous formation due to high consumption of salted tea may be a critical risk factor for the high occurrence of oesophageal and gastric cancers in Kashmir.

Bicarbonates↗
PubMed1979

Effect of transverse tubule-disruption on 14C-caffeine influx in frog skeletal muscle.

Effect of transverse tubule-disruption (T-disruption) on 14C-caffeine influx was studied using small bundles, consisting of 40 to 50 fibers, of frog semitendinosus muscle. The peak tension of caffeine contracture was inhibited by about 69% at 5 mM caffeine and by about 31% at 7 mM caffeine by T-disruption. In addition, the amount of caffeine influx in a small bundle was inhibited by about 52% at 5 mM caffeine and by about 28% at 7 mM caffeine by T-disruption, corresponding to the inhibition of the peak tension of caffeine contracture by T-disruption. These findings support our previous suggestion that caffeine enters the muscle fibers through the surface membrane and transverse tubuler membrane (T-membrane), and that the T-membrane contributes to the entry of caffeine more greatly at 5 mM caffeine than at 7 mM caffeine. Moreover, at 5 mM caffeine it was noted that there is a slight difference between the extent of inhibition of the caffeine influx and that of the peak contracture tension. From these results, it could be concluded that the inhibition of peak tension of caffeine contracture by T-disruption is mainly due to the inhibition of caffeine influx which occurs through the T-membrane and is partly due to the functional disturbance of the sarcoplasmic reticulum which is probably induced by T-disruption.

Animals↗
PubMed1992

Caffeine-induced release and reuptake of Ca2+ by Ca2+ stores in myocytes from guinea-pig urinary bladder.

1. Voltage-clamped isolated smooth muscle cells from guinea-pig urinary bladder were studied with 3.6 mM extracellular Ca2+ at 36 degrees C. The fluorescence of the Ca(2+)-sensitive dye Indo-1 was used to monitor the cytosolic calcium concentration ([Ca2+]i) and its changes ([Ca2+]i transient). Fast application of caffeine (10 mM) to the cell was used to release the intracellular Ca2+ from a 'caffeine-sensitive Ca2+ store'. 2. At the holding potential -60 mV, a short (1 s) caffeine application increased [Ca2+]i within less than 1 s from the resting 118 +/- 22 nM to 1490 +/- 332 nM. Following the caffeine wash-out, [Ca2+]i fell from this peak to a subresting level of 47 +/- 12 nM, i.e. an 'undershoot' of [Ca2+]i occurred. Subsequent caffeine-induced [Ca2+]i transients had attenuated peaks suggesting that the caffeine-sensitive Ca2+ store had lost a part of the releasable Ca2+. 3. In the continuous presence of caffeine, [Ca2+]i decayed from its peak to control resting [Ca2+]i values. The wash-out of caffeine following prolonged (10-30 s) treatment also resulted in [Ca2+]i undershoot. Subsequent caffeine-induced [Ca2+]i transients were largely abolished as if the caffeine-sensitive Ca2+ store had lost a large part of releasable Ca2+. During the undershoot, hyperpolarization to -100 mV did not affect [Ca2+]i. In most cells studied, recovery of [Ca2+]i from the undershoot to the resting level required depolarizations inducing Ca2+ influx through L-type Ca2+ channels. 4. Block of plasmalemmal Ca(2+)-ATPase (PMCa) with extracellular La3+ (3 mM) did not modify the decay of the [Ca2+]i transients induced by depolarization or by a 1 s caffeine application suggesting that decay rate of both is not limited by PMCa rate. La3+ abolished the undershoot of [Ca2+]i. In the continuous presence of caffeine, La3+ largely prevented the decay of [Ca2+]i. 5. When the depolarizing steps from -60 to 0 mV (160 ms duration) were applied during the period of [Ca2+]i undershoot, the half-time of decay of the corresponding [Ca2+]i transients was up to three times faster than in control. Repetitive depolarizations restored the rate of decay and [Ca2+]i recovered to the resting value. Both processes recovered along a similar time course. 6. Application of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX; 0.1 mM) or of 8-Br-cAMP (0.1 mM) did not mimic the above caffeine effects suggesting that stimulation of sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCa) by cAMP-dependent phosphorylation is not the underlying mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1992

Mechanisms of caffeine-induced contraction and relaxation of rat aortic smooth muscle.

1. Using front-surface fluorimetry and Fura-2, we determined the effects of caffeine on cytosolic calcium concentration ([Ca2+]i) and on tension of strips of the rat thoracic aorta. We also determined the effects of caffeine on 45Ca2+ influx into the strips. The objective was to elucidate the mechanism of contraction and relaxation in vascular smooth muscle, as induced by caffeine. 2. In normal physiological salt solution (PSS), caffeine induced a transient tension development, while it induced a biphasic change in [Ca2+]i. The initial transient peak in [Ca2+]i which coincided with tension development was followed by a sustained increase. Thus, changes in tension did not follow changes in [Ca2+]i. In Ca(2+)-free PSS, both the caffeine-induced contraction and the increase in [Ca2+]i were transient. It was suggested that in both the presence and absence of extracellular Ca2+, the transient increase in [Ca2+]i was due to the release of Ca2+ from the intracellular store. Although the sustained increase in [Ca2+]i depended on extracellular Ca2+, it was not affected by diltiazem, a Ca2+ antagonist. 3. Caffeine inhibited the increase in [Ca2+]i and tension development during 118 mM-K+ depolarization, in a concentration-dependent manner. The extent of reduction in tension (relaxation) was greater than that expected from the reduction in [Ca2+]i based on the [Ca2+]i-tension relationship observed with K+ depolarization. Pretreatment of the strips with ryanodine did not alter the inhibitory effects of caffeine. 4. Caffeine inhibited the increased [Ca2+]i and developed tension during stimulation by 10(-5) M-noradrenaline, in a concentration-dependent manner. 5. Dibutyryl cAMP (10(-4) M) inhibited both high K(+)-induced and noradrenaline-induced tension development. Inhibition of an increase in [Ca2+]i in relation to the inhibition of tension during noradrenaline stimulation was much greater than that in 118 mM-K+ depolarization. 6. Although caffeine per se had no effect on 45Ca2+ influx in the strips in normal PSS, caffeine did inhibit the increase in 45Ca2+ influx stimulated by 118 mM-K+ or by 10(-5) M-noradrenaline, to a similar extent and with similar IC50 values. 7. The characteristic features of the effects of caffeine on vascular smooth muscle, i.e. the transient nature of contraction and the relaxation of precontracted strips could be explained as follows: caffeine is able to reduce [Ca2+]i after releasing Ca2+ from intracellular stores; however, this may play a minor role. Independent of the [Ca2+]i reduction, the second messenger, cAMP, might directly influence the [Ca2+]i-tension relationship, and if so, would play a major role.

Animals↗
PubMed1975

Contractures in partially depolarized muscle treated with caffeine or nitrate.

Frog toe muscles partially depolarized with a subcontracture concentration (15 or 20mM) of K+ rapidly developed tension when exposed to 1 mM caffeine, which alone did not cause contracture. This action resulted from a lowering of the mechanical threshold by the caffeine and thus was similar to that caused by replacement of Cl- with NO3-. Maximal tension was the same in the caffeine and NO3- media but took much longer to develop in the former. Equilibrating the muscles with caffeine for 60 s (the time calculated for complete diffusion) did not reduce contraction time significantly. However, prolonging the exposure of muscles to caffeine beyond this time enhanced the drug's capacity to potentiate both the twitch and 30 mM K+ contractures and shortened the contraction time of the contractures. Toe muscles that had undergone a contracture in 100 mM K+ and were recovering in 15 mM K+-Ringer generated tension in the presence of 1 mM caffeine or NO3- but only after enough repolarization had been achieved so that a response to a second challenge with 100 mM K+ could be demonstrated. Although prolonged immersion in the K+-enriched recovery solution caused a disappearance of sensitivity to a test depolarization, addition of 1 mM caffeine or replacement of Cl- with NO3- promptly evoked a contracture. These results imply a reversible step in the recovery process that is both potential and time dependent. Since application of 5 mM caffeine to either normally polarized or depolarized muscles always immediately causes contracture, more than one site of action for caffeine is indicated. After disruption of the transverse tubules, partially depolarized muscles showed no response to NO3- or 1 mM caffeine but contracted vigorously when exposed to 5 mM caffeine.

Action Potentials↗