Long-term caffeine inhibits Ehrlich ascites carcinoma cell-induced induction of central GABAergic activity.
01 Nov 2000-Neurochemical Research (Kluwer Academic Publishers-Plenum Publishers)-Vol. 25, Iss: 11, pp 1457-1463
TL;DR: It may be concluded that caffeine (adenosine receptor antagonist) suppresses the EAC cell-induced induction of whole brain GABAergic activity in mice.
Abstract: Long-term administration (for 22-27 consecutive days) of caffeine (20 mg/kg/day p.o) developed tolerance to this drug by upregulating the central GABAergic activity. Development of Ehrlich ascites carcinoma (EAC) cell induced the whole brain GABAergic activity. But pretreatment of caffeine and continuation of its treatment in the course of development of EAC cells restored the EAC cell-induced change of GABAergic activity to control values. Thus, it may be concluded that caffeine (adenosine receptor antagonist) suppresses the EAC cell-induced induction of whole brain GABAergic activity in mice.
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TL;DR: The results demonstrate that ERAE and its major compound, evodiamine, provide an excellent candidate for the treatment or prevention of caffeine-induced sleep disturbances and excitatory states, and that the mechanism of these beneficial effects acts, at least in part, through the GABAA-ergic system.
Abstract: Worldwide, caffeine is among the most commonly used stimulatory substances. Unfortunately, significant caffeine consumption is associated with several adverse effects, ranging from sleep disturbances (including insomnia) to cardiovascular problems. This study investigates whether treatment with the Evodia rutaecarpa aqueous extract (ERAE) from berries and its major molecular component, evodiamine, can reduce the adverse caffeine-induced sleep-related and excitation effects. We combined measurements from the pentobarbital-induced sleep test, the open field test, and the locomotor activity test in mice that had been dosed with caffeine. We found that ERAE and evodiamine administration reduced the degree of caffeine-induced sleep disruption during the sleep test. Additionally, we found that evodiamine significantly inhibits caffeine-induced excitation during the open field test, as well as decreasing hyperlocomotion in the locomotor activity test. Additional in vitro experiments showed that caffeine administration decreased the expression of γ-aminobutyric acid (GABA)A receptor subunits in the mouse hypothalamus. However, evodiamine treatment significantly reversed this expression reduction. Taken together, our results demonstrate that ERAE and its major compound, evodiamine, provide an excellent candidate for the treatment or prevention of caffeine-induced sleep disturbances and excitatory states, and that the mechanism of these beneficial effects acts, at least in part, through the GABAA-ergic system.
17 citations
Cites background from "Long-term caffeine inhibits Ehrlich..."
...Treatment with caffeine, however, suppresses the expression of GABAergic systems and results in sleep disturbances (Mukhopadhyay and Poddar, 2000; Li et al., 2004; Mabunga et al., 2015)....
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TL;DR: It is suggested that long‐term caffeine intake may inhibit or reverse the EAC cell‐induced immune suppression, including the HPA axis biomarker.
Abstract: The aim of this study was to investigate the effect of long-term consumption of caffeine in the development of Ehrlich ascites carcinoma (EAC) cells in adult female mice, 25–30 g, in relation to immune response. Mice were treated with caffeine (20 mg kg−1 daily, p.o.) for 22–27 consecutive days or inoculated with EAC cells (5 times 106 cells/mL, i.p.), or both. Control mice, corresponding to experimental groups, were treated with corresponding vehicles under similar conditions. The lymphocyte viability, mitogen-induced proliferating activity, cytotoxicity and DNA fragmentation from blood, spleen and thymus of both control and experimental groups were measured as immune response parameters. An immune response index, corticosterone, was also measured in adrenals and plasma under similar conditions. Results showed that development of EAC cells caused immune suppression with a reduction of lymphocyte viability, cytotoxicity and proliferative activity and induction of DNA fragmentation in those tissues, as well as an increase in plasma corticosterone. Though long-term caffeine treatment (which resulted in tolerance to caffeine) alone did not alter significantly any of the immune response parameters studied, including corticosterone status (immune biomarker), the continuation of caffeine treatment during the development of EAC cells either restored or reduced the EAC cell-induced alteration in these parameters, including the HPA axis biomarker. These results suggest that long-term caffeine intake may inhibit or reverse the EAC cell-induced immune suppression.
7 citations
Cites background or methods from "Long-term caffeine inhibits Ehrlich..."
...…a variety of cancers such as ovarian, lung, skin and breast cancer, including Ehrlich ascites tumour development, has been reported from our laboratory (Mukhopadhyay & Poddar 2000, 2001; Mandal et al 2007) as well as by others (Theiss & Shimkim 1978; VanderPloeg & Welsch 1991; Conney et al 2002)....
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...Mice were grouped and treated accordingly as described elsewhere (Mukhopadhyay & Poddar 2000)....
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...Mukhopadhyay & Poddar (2000) and Mandal et al (2007) have also reported that caffeine may mediate its action through interaction with the HPA- and HPG-axis involving excitatory and inhibitory neurotransmitters, neuropeptides and neurotrophic hormones, including LH and FSH. Ramanaviciene et al…...
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...…development of tolerance to caffeine, which has been supported by the observations at the level of locomotor activity as well as by hypothalamic GABA-ergic activity under similar conditions of caffeine treatment with respect to the corresponding control (Mukhopadhyay & Poddar 1998, 2000, 2001)....
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...In recent past reports, authors have shown that caffeine affects the hypothalamo-pituitary-gonadal axis (HPG), hypothalamopituitary-adrenal axis (HPA) and central GABA-ergic activity (Spindel et al 1980; Ezzat & El-Gohary 1994; Mukhopadhyay & Poddar 2000; Mandal et al 2007)....
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Journal Article•
TL;DR: It is suggested that prolonged caffeine exposures may inhibit the development of EAC cell through the reduction or restoration of Eac cell-induced disruption of ovarian hormonal status to their normal status via the modulation of Hypothalamic-Pituitary-Gonadal (HPG) axis.
Abstract: Inhibitory action of caffeine (a tri-methylxanthine alkaloid) on progression or pathogenesis of lung, breast and ovarian cancer including Ehrlich ascites carcinoma (EAC) cell development has been reported. This information led the authors to study the effect of long-term administration of caffeine (20 mg/kg/day; po for 22-27 consecutive days) on the development of EAC cells in relation to serum gonadal hormones (LH, FSH, 17-OH-beta-estradiol (E2) and progesterone) in adult Swiss albino female mice. Measurement of gonadal hormones in serum using RIA showed that (a) long-term caffeine treatment significantly increased LH (except for 27 consecutive days) and decreased FSH (except for 24 and 27 consecutive days) and both E2 and progesterone (except for 22 and 24 consecutive days) levels, (b) development of EAC cell for 10-15 days, significantly increased LH but decreased FSH, E2 and progesterone levels and (c) long-term caffeine consumption during the development of EAC cell (i) restored the EAC cell- or caffeine-induced induction of LH and reduction of FSH level to their normal levels and (ii) withdrew/reduced the EAC cell-induced reduction in only E2 but not progesterone level. These results therefore, suggest that prolonged caffeine exposures may inhibit the development of EAC cell through the reduction or restoration of EAC cell-induced disruption of ovarian hormonal status to their normal status via the modulation of Hypothalamic-Pituitary-Gonadal (HPG) axis.
6 citations
References
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TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
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TL;DR: This chapter reviews the human pharmacology of caffeine; the evidence for its role in causing human disease, including addiction; and its potential usefulness as a therapeutic agent.
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TL;DR: It has been found that certain amino acids and indole derivatives, when allowed to react with ninhydrin at an alkaline pHS, form highly fluorescent products that can be measured in as little as 3 ,ug dry weight of brain tissue.
Abstract: THE uniquely high activity of glutamic decarboxylase (GDC)? in brain has been reported (ROBERTS, 1950; WINGO and AWAPARA, 1950). ROBERTS (1956), using pooled tissues, has shown that there is a fiveto six-fold greater activity of GDC in grey matter than in white matter of the cat brain. Because of the limitations of the manometric methods used, further resolution of the cytoarchitectonic distribution of GDC has awaited the development of more sensitive analytical methods for measuring the activity of this enzyme. It has been found that certain amino acids and indole derivatives, when allowed to react with ninhydrin at an alkaline pHS, form highly fluorescent products. Of the substances tested, under the conditions to be described, y-aminobutyric acid (yAB) has given the greatest amount of fluorescence and can be measured at a concentration of lo-' M. A fluorescence method has been developed to measure the activity of GDC in as little as 3 ,ug dry weight of brain tissue. The activity of this enzyme has been measured in various areas of the monkey and rabbit brain as well as in the whole brain of mouse and rat. The histochemical distribution of GDC in the layers of the monkey cerebellar cortex and selected white tracts of the rabbit and rat has also been determined. White matter has been shown to be extremely poor in GDC.
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"Long-term caffeine inhibits Ehrlich..." refers background in this paper
...Development of implanted inducible tumors is a result of stress (9,10)....
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...Since the growth of implanted tumors is a result of inescapable stress (9,10) and stress (a) induces the rapid synthesis of GABA binding sites or may induce dissociation of one or more of the endogenous inhibitors of GABA binding which include occluded GABA bound to cryptic receptors, phospholipids and peptides (11,29) and (b) modulate GABA activation of Cl − ion influx (12), it may be suggested that development of EAC cell in mice induces stress which may activate the brain GABAergic activity....
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