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PubMed1995

Effects of caffeine on cognition and mood without caffeine abstinence.

The objective of this study was to evaluate the effects of low doses (75 mg and 150 mg) of caffeine on mood and cognition in healthy people, with minimal abstinence of 1 h from caffeine. Improvements were obtained in cognition for attention, problem solving and delayed recall, but not immediate recall or working memory, but performance in the placebo condition was close to the maximum, giving little margin for improvement. For mood, there were statistically significant increase in clearheadedness, happiness and calmness and decreases in tenseness. These mood and performance-enhancing effects of caffeine cannot be seen as representing an alleviation of deficits induced by caffeine abstinence, because there was only minimal deprivation from caffeine.

Adolescent↗

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↗

PubMed1989

Anxiolytic effect of caffeine and caffeine-clonazepam interaction: evaluation by NaCl solution intake.

The administration of drugs with anxiolytic action to rehydrating rats augments the intake of 1.5% NaCl solution. In order to clarify the status of caffeine as an anxiolytic agent and its possible interaction with a benzodiazepine having high potency and efficacy in this regard, caffeine (0.78-100 mg/kg) alone and caffeine (0.78-50 mg/kg) plus clonazepam (0.05 or 0.50 mg/kg) injections (IP) were administered to rehydrating rats prior to 1-hr sessions during which they drank 1.5% NaCl solution. When given alone, caffeine, within a particular dose range, and clonazepam at both doses, augmented NaCl solution intake, but when administered in combination, caffeine antagonized the effects of clonazepam.

Animals↗

PubMed1997

Caffeine vs caffeine-free sports drinks: effects on urine production at rest and during prolonged exercise.

We compared the effects of caffeinated vs non-caffeinated carbohydrate electrolyte (CE) drinks on urine volume (UV), free water clearance (CH2O), fractional excretion of water (FEH2O), and osmolar excretion during 4 h of rest or 1 h rest followed by 3 h of cycling at 60% VO2max in six subjects. We also tested maximal performance at 85% VO2max following the 3-h exercise trials. Throughout the two resting trials and the two rest + exercise trials, subjects ingested CE (total volume = 35 ml/kg) without (PLAC) or with (CAFF) caffeine (25 mg/dl). Blood samples were collected, and body weight and UV were recorded every hour. Urine and blood were analyzed for osmolality and creatinine, and plasma catecholamine concentrations were determined. At rest, mean (+/-SE) UV between 60 min and 240 min was greater for CAFF (1843 +/- 166 ml) vs PLAC (1411 +/- 181 ml) (p < 0.01); during exercise the difference in UV between CAFF (398 +/- 32 ml) and PLAC (490 +/- 57 ml) was not significant. Cycling performance was unaffected by caffeine. Plasma catecholamine concentrations were not different between PLAC and CAFF but were greater during exercise than rest (p < 0.01) and may have counteracted the diuretic effect of caffeine observed at rest. Thus, CAFF consumed in CE during moderate endurance exercise apparently does not compromise bodily hydration status.

Adult↗

PubMed1988

Endogenous adenosine and hemorrhagic shock: effects of caffeine administration or caffeine withdrawal.

Plasma adenosine concentrations doubled when rats were subjected to 90 min of profound hemorrhagic shock. Administration of caffeine (20 mg per kg of body weight), an adenosine-receptor antagonist, attenuated the hemorrhage-induced decrease in blood pressure. In contrast, chronic caffeine consumption (0.1% in drinking water), followed by a brief period of caffeine withdrawal, amplified the hypotensive response to hemorrhage. These data suggest that endogenous adenosine participates in the hypotensive response to hemorrhage and that caffeine may protect against, and caffeine withdrawal may exacerbate, this response.

Adenosine↗

PubMed1981

Ad lib caffeine consumption, symptoms of caffeinism, and academic performance.

The authors explored the relationship between ad lib caffeine consumption in college students and the incidence of caffeinism, characterized by heightened anxiety, depression, and various psychophysiological reactions. Students were randomly selected from four groups (abstainers from caffeine and low, moderate, and high consumers). A survey battery assessed the effects of caffeine, incidence of psychophysiological disorders, state-trait anxiety, and depression. The moderate and high consumer groups combined reported significantly higher trait anxiety and depression scores when compared with abstainers. The high consumer group also reported significantly higher levels of symptoms of caffeinism, higher frequency of psychophysiological disorders, and lower academic performance.

Age Factors↗

PubMed1989

Biochemical and enzymatic aspects of caffeine and caffeine derivatives induced DNA strand breaks.

The results presented here point to the difficulties that exist in connection with the identification of the molecular target of caffeine. Our data support the evidence that caffeine and caffeine derivatives cause DNA-protein cross-links (DPC) in whole mammalian cells or in isolated nuclei. These DPC have the same properties (saturability, reversibility and temperature-dependence) as those produced by an enzymatic inhibition. The experiments performed in reconstituted systems, in the presence of purified DNA topoisomerase II, do not support the original hypothesis that this enzyme might be a possible target for this class of drugs. We suggest the possibility that other DNA metabolism enzymes are involved in the biological effects of caffeine and caffeine derivatives. Further biochemical and molecular data are necessary to identify which of these enzymes is in fact affected.

Animals↗

PubMed1997

The effect of caffeine and caffeine analogs on rat liver phosphorylase a activity.

Liver phosphorylase a is stimulated by adenosine monophosphate. It is inhibited by adenosine diphosphate, adenosine triphosphate and glucose. Using these effectors as well as other potential in vivo effectors at concentrations approximating those present in hepatocytes, we previously reported that the net effect was nil, i.e., at estimated in vivo concentration, the inhibitors neutralized the stimulatory effect of adenosine monophosphate in a phosphorylase a preparation. In addition, a concentration dependent inhibition by glucose was not present. Therefore, we were interested in determining if addition of caffeine, an inhibitor that synergizes with glucose, would result in a reduction in activity in the presence of the other effectors and restore regulation by physiological concentrations of glucose. The effect of xanthine and xanthine analogs also were studied. Purified liver phosphorylase a was used. Activity was measured in the direction of glycogenolysis at 37 degrees, pH 7.0 and under initial rate conditions. Caffeine (1 mM) was added to individual and various combinations of other effectors. The interactions among the potential in vivo effectors when caffeine was present were complex. However, when caffeine was present glucose again regulated activity. This most likely was due to a synergistically facilitated reduction in binding affinity for AMP by caffeine and glucose. Theophylline and adenosine did not inhibit activity but reduced AMP stimulation and facilitated glucose inhibition. Xanthine and the other xanthine derivatives all strongly inhibited activity and the inhibition was independent of other effectors.

Adenine Nucleotides↗

PubMed1988

Caffeine interaction with the Ca-release channels of heavy sarcoplasmic reticulum. Evidence that 170 kD Ca-binding protein is a caffeine receptor of the Ca-channels.

The study of Ca2+- and caffeine-induced Ca2+ release from heavy sarcoplasmic reticulum vesicles under the different conditions suggests that Ca2+ and caffeine can interact with the common receptor of the Ca-release channels. The reticulum membranes were solubilized using nonionic detergent polyoxyethylene 9-lauryl ether, and affinity chromatography on reactive red 120-agarose was carried out. The 170 kD Ca-binding protein which is eluted by caffeine is the most probable candidate for the caffeine receptor of the Ca-channels.

Animals↗

PubMed1980

On the interaction of caffeine with nucleic acids. IV. Studies of the caffeine-DNA interaction by infrared and ultraviolet linear dichroism, proton and deuteron nuclear magnetic resonance.

The DNA-caffeine interaction at high concentration of caffeine (Cf) leads to an arrangement of Cf molecules outside of the DNA double helix with an orientation parallel to the bases both in the A and B form as demonstrated by infrared linear dichroism. Addition of DNA broadens the 1H NMR lines of Cf in aqueous solution indicating a specific binding. Intercalation is not the predominant mechanism, the deuterium relaxation time T1 = (38 +/- 7) ms and the estimated reorientation correlation time tau cb = 0.17 ns of caffeine-8[2H] in the Cf-DNA complex suggest an outside stacking of the ligand. According to the results a model on the DNA-Cf complex at high Cf concentration (binding process II) is suggested including the caffeine-induced reorientation of the hydration shell of DNA.

Caffeine↗

PubMed2005

Inhibition of HIV-1 replication by caffeine and caffeine-related methylxanthines.

Human immunodeficiency virus type I (HIV-1) DNA integration is an essential step of viral replication. We have suggested recently that this stage of HIV-1 life-cycle triggers a cellular DNA damage response and requires cellular DNA repair proteins for its completion. These include DNA-PK (DNA-dependent protein kinase), ATR (ataxia telangiectasia and Rad3-related), and, at least in some circumstances, ATM (ataxia telangiectasia mutated). Host cell proteins may constitute an attractive target for anti-HIV-1 therapeutics, since development of drug resistance against compounds targeting these cellular cofactor proteins is unlikely. In this study, we show that an inhibitor of ATR and ATM kinases, caffeine, can suppress replication of infectious HIV-1 strains, and provide evidence that caffeine exerts its inhibitory effect at the integration step of the HIV-1 life-cycle. We also demonstrate that caffeine-related methylxanthines including the clinically used compound, theophylline, act at the same step of the HIV-1 life-cycle as caffeine and efficiently inhibit HIV-1 replication in primary human cells. These data reveal the feasibility of therapeutic approaches targeting host cell proteins and further support the hypothesis that ATR and ATM proteins are involved in retroviral DNA integration.

Ataxia Telangiectasia Mutated Proteins↗

PubMed1998

Strain differences in CYP3A-mediated C-8 hydroxylation (1,3,7-trimethyluric acid formation) of caffeine in Wistar and Dark Agouti rats. Rapid metabolism of caffeine in debrisoquine poor metabolizer model rats.

We observed significant strain differences [Dark Agouti (DA) > Wistar] in 1,3,7-trimethyluric acid formation (C-8 hydroxylation) during caffeine metabolism, though not in N-demethylations, in adult male DA and Wistar rats. In contrast, adult female and immature male rats of both DA and Wistar strains did not show significant differences in activity levels of C-8 hydroxylation. Kinetic studies using liver microsomes revealed that adult male DA rats have a larger Vmax for C-8 hydroxylation than do Wistar rats. Troleandomycin (TAO), known as a cytochrome P450 (CYP) 3A inhibitor, and an anti-rat CYP3A2 polyclonal antibody effectively reduced C-8 hydroxylation by rat liver microsomes in a concentration-dependent manner, suggesting that C-8 hydroxylation in rats is mediated largely by an isoform(s) of the CYP3A subfamily. Troleandomycin and the antibody did not inhibit the N-demethylations of caffeine by rat liver microsomes. Treatment of rats with CYP3A inducers caused a marked increase in C-8 hydroxylase activity. These results indicate that the rat CYP3A subfamily is capable of catalyzing C-8 hydroxylation of caffeine as is the case for human CYP3A4. The results of western blotting analysis using anti CYP3A antiserum showed that the staining intensity of the protein band in DA rat liver microsomes was higher than that in Wistar rat liver microsomes. We concluded that marked sex-dependent strain differences in C-8 hydroxylation of caffeine between Wistar and DA rats are due to the differences in the levels of expression of CYP3A in these strains of rats.

Aging↗

PubMed2003

The first committed step reaction of caffeine biosynthesis: 7-methylxanthosine synthase is closely homologous to caffeine synthases in coffee (Coffea arabica L.).

In coffee and tea plants, caffeine is synthesized from xanthosine via a pathway that has three methylation steps. We identified and characterized the gene encoding the enzyme for the first methylation step of caffeine biosynthesis. The full-length cDNA of coffee tentative caffeine synthase 1, CtCS1, previously isolated by the rapid amplification of cDNA ends was translated with an Escherichia coli expression system and the resultant recombinant protein was purified using Ni-NTA column. The protein renamed CmXRS1 has 7-methylxanthine synthase (xanthosine:S-adenosyl-L-methionine methyltransferase) activity. CmXRS1 was specific for xanthosine and xanthosine 5'-monophosphate (XMP) could not be used as a substrate. The K(m) value for xanthosine was 73.7 microM. CmXRS1 is homologous to coffee genes encoding enzymes for the second and third methylation steps of caffeine biosynthesis.

Caffeine↗

PubMed1998

Evaluation of the developmental toxicity of caffeine and caffeine metabolites using the frog embryo teratogenesis assay--Xenopus (FETAX).

The developmental toxicities of caffeine and 13 metabolites, including theophylline, and paraxanthine and a synthetic methylxanthine analogue 3-isobutyl-methylxanthine (IBMX) were evaluated using the Frog Embryo Teratogenesis Assay Xenopus (FETAX). Young X. laevis embryos were exposed to these compounds in each of two separate concentration-response experiments with and without an exogenous metabolic activation system (MAS). Results obtained from these studies indicated that relative teratogenic potencies of caffeine and each of its di- and monomethylxanthine metabolites were similar. Representatives of both the substituted uric and uracil metabolites were less developmentally toxic on an equimolar basis than the methylxanthines, suggesting that they may have represented detoxification metabolites. IBMX, a phosphodiesterase inhibitor also known to be an adenosine receptor antagonist, was the most potent developmental toxicant of the materials evaluated. In conclusion, none of the caffeine metabolites tested was found to be significantly more potent than caffeine itself in the FETAX assay.

Abnormalities, Drug-Induced↗

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↗

PubMed1988

Caffeine post-treatment causes a shift in the chromosome aberration types induced by mitomycin C, suggesting a caffeine-sensitive mechanism of DNA repair in G2.

Human lymphocytes were exposed in G1 to mitomycin C (2.5 microM for 2 h) and harvested at 3-h intervals from 48 to 84 h after stimulation. All cultures were also post-treated in G2 with caffeine (2 mM). Different types of chromosomal aberrations were scored in the first division metaphases. Caffeine increases all chromosome aberration types by promoting a premature mitosis of damaged cells. However, when the frequency of damaged cells is not affected by the caffeine post-treatment, a reduction of the frequency of the exchange-type aberrations was shown. The possibility that caffeine interferes with some mechanism of G2 repair is discussed.

Caffeine↗

PubMed1991

Pharmacogenetics of caffeine and caffeine-halothane contractures in biopsies of human skeletal muscle.

In vitro pharmacological responses of fresh biopsy specimens of human skeletal muscle were used as indicators of some intrinsic muscle properties. The measured parameters that were utilized for the current study were contractures induced in vitro by caffeine or by caffeine plus halothane. The opportunity to study such specimens arose from clinical testing for diagnosing the genetic predisposition to malignant hyperthermia, a potentially fatal complication of anaesthesia. The current analysis covers data from over 1,000 subjects, most of whom were clinical suspects and relatives of these. Responsiveness of the muscle specimens varied over two orders of magnitude. The frequency distribution curves suggest that the variation does not represent a continuum but that there are three or more clusters of functional variants. Muscle specimens from males were on average more responsive to caffeine than were those from females. Correlations within father-son and brother-brother pairs indicated complete heritability of responsiveness; this might have been expected but the surprise was a lack of correlation within mother-daughter pairs. There was an intermediate correlation in father-daughter pairs. The sex difference in heritability could be due to gender-related modifying genes or due to secondary modification of the muscle response in females by sex-related, perhaps hormonal factors. Among the effects of age appeared to be poor development in early childhood of the potentiation of the caffeine contracture by halothane.

Adolescent↗