CYBERMED LIFE - ORGANIC  & NATURAL LIVING

Acetaminophen

  • Acetaminophen

  • Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro.

    facebook Share on Facebook
    Abstract Title:

    Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro.

    Abstract Source:

    Int J Biochem Cell Biol. 2005 Aug ;37(8):1727-37. Epub 2005 Apr 26. PMID: 15878691

    Abstract Author(s):

    Svetlana Dimova, Peter H M Hoet, David Dinsdale, Benoit Nemery

    Article Affiliation:

    Svetlana Dimova

    Abstract:

    Recent epidemiological observations suggest that acetaminophen (paracetamol) may contribute to asthma morbidity. Impaired endogenous antioxidant defences may have a role in the pathogenesis of a number of inflammatory pulmonary diseases, including asthma. We studied the effect of acetaminophen on the intracellular level of reduced glutathione (GSH) with and without inhibitors of cytochrome P450 or prostaglandin H synthetase, and TNF-alpha, IL-6 and IL-8 protein production in human alveolar macrophages and type II pneumocytes in vitro. Following a 20 h incubation with acetaminophen, cytotoxicity was apparent from>or = 5 and>or = 10 mM in macrophages and type II pneumocytes, respectively. A time- and concentration-dependent decrease of intracellular GSH occurred after acetaminophen (0.05-1 mM) exposure (1-4 h) in pulmonary macrophages (up to 53%) and type II pneumocytes (up to 34%). Diethyldithiocarbamic acid, potassium ethyl xanthate, and indomethacin decreased significantly acetaminophen-induced GSH depletion in the two cell types tested, suggesting the involvement of cytochrome P450 (mainly CYP2E1) and/or prostaglandin H synthetase. In macrophages, acetaminophen decreased the secretion of TNF-alpha (at 4 and 24 h, concentration-related) and IL-6 (at 24 h, at 0.1 mM), and did not affect significantly IL-8 production. These in vitro observations demonstrate that clinically relevant concentrations of acetaminophen decreased: (i) intracellular GSH in human pulmonary macrophages and type II pneumocytes and (ii) the secretion of TNF-alpha and possibly IL-6 by human pulmonary macrophages. These findings provide experimental plausibility to the challenging observations that frequent use of APAP may be a risk factor for asthma morbidity.

  • Ascorbic acid prevents acetaminophen-induced hepatotoxicity in mice by ameliorating glutathione recovery and autophagy.

    Abstract Title:

    Ascorbic acid prevents acetaminophen-induced hepatotoxicity in mice by ameliorating glutathione recovery and autophagy.

    Abstract Source:

    Arch Biochem Biophys. 2016 Jun 7. Epub 2016 Jun 7. PMID: 27288086

    Abstract Author(s):

    Toshihiro Kurahashi, Jaeyong Lee, Atsunori Nabeshima, Takujiro Homma, Eun Sil Kang, Yuka Saito, Sohsuke Yamada, Toshiyuki Nakayama, Ken-Ichi Yamada, Satoshi Miyata, Junichi Fujii

    Article Affiliation:

    Toshihiro Kurahashi

    Abstract:

    Aldehyde reductase (AKR1A) plays a role in the biosynthesis of ascorbic acid (AsA), and AKR1A-deficient mice produce about 10-15% of the AsA that is produced by wild-type mice. We found that acetaminophen (AAP) hepatotoxicity was aggravated in AKR1A-deficient mice. The pre-administration of AsA in the drinking water markedly ameliorated the AAP hepatotoxicity in the AKR1A-deficient mice. Treatment of the mice with AAP decreased both glutathione and AsA levels in the liver in the early phase after AAP administration, and an AsA deficiency delayed the recovery of the glutathione content in the healing phase. While in cysteine supply systems; a neutral amino acid transporter ASCT1, a cystine transporter xCT, enzymes for the transsulfuration pathway, and autophagy markers, were all elevated in the liver as the result of the AAP treatment, the AsA deficiency suppressed their induction. Thus, AsA appeared to exert a protective effect against AAP hepatotoxicity by ameliorating the supply of cysteine that is available for glutathione synthesis as a whole. Because some drugs produce reactive oxygen species, resulting in the consumption of glutathione during the metabolic process, the intake of sufficient amounts of AsA would be beneficial for protecting against the hepatic damage caused by such drugs.

  • The beneficial effects of ozone therapy in acetaminophen-induced hepatotoxicity in mice.

    facebook Share on Facebook
    Abstract Title:

    The beneficial effects of ozone therapy in acetaminophen-induced hepatotoxicity in mice.

    Abstract Source:

    Pharmacol Rep. 2017 Nov 13 ;70(2):340-345. Epub 2017 Nov 13. PMID: 29477043

    Abstract Author(s):

    Aysu Hayriye Tezcan, Omur Ozturk, Sefer Ustebay, Yasemen Adali, Hatice Yagmurdur

    Article Affiliation:

    Aysu Hayriye Tezcan

    Abstract:

    BACKGROUND:The aim of the present study was to determine the therapeutic effects of medical ozone therapy on acute acetaminophen (APAP)-induced hepatotoxicity which were not clearly demonstrated in prior studies.

    METHOD:Twenty-four mice were randomly assigned into three equal groups: Group 1 (control), Group 2 (APAP) and Group 3 (APAP +ozone). Hepatotoxicity was induced by APAP given as a single dose of 300 mg/kg intraperitoneally in Groups 2 and 3. Additionally, Group 3 received 20 mcg/0.5 mL ozone intraperitoneal twice a day for the remaining of the study. Other groups received saline injections. On the fourth day of the study, biochemical variables (AST, ALT, ALP) and liver histopathology wasassessed.

    RESULTS:Intraperitoneal administration of a single dose of APAP induced hepatocellular damage that was shown by both liver enzymes and histopathological changes (p < 0.001). AST, ALT, ALP levels were elevated in both groups 2 and 3 and the difference from group 1 was statistically significant (p < 0.01).Mean ALT and AST levels of group 2 were statistically significantly higher versus group 3 (p < 0.01). In histopathological examinations; necrosis and inflammation were more prominent in Group 2 compared to Group 3 (p < 0.01).

    CONCLUSION:Ozone showed beneficial effects on APAP hepatotoxicity at a statistically significant level. It is known that ozone has therapeutic effects in various diseases owing to its antioxidant effects. The present study suggests that ozone may be utilized as a routine supplementary therapy in acute APAP hepatotoxicity.

  • The effects of acupuncture after thyroid surgery: A randomized, controlled trial.

    facebook Share on Facebook
    Abstract Title:

    The effects of acupuncture after thyroid surgery: A randomized, controlled trial.

    Abstract Source:

    Surgery. 2014 Dec ;156(6):1605-12; discussion 1612-3. Epub 2014 Nov 11. PMID: 25456960

    Abstract Author(s):

    Maurizio Iacobone, Marilisa Citton, Simone Zanella, Marco Scarpa, Giulia Pagura, Saveria Tropea, Helmut Galligioni, Francesco Ceccherelli, Paolo Feltracco, Giovanni Viel, Donato Nitti

    Article Affiliation:

    Maurizio Iacobone

    Abstract:

    BACKGROUND:Acupuncture is a safe and well-tolerated treatment for pain relief. Previous studies supported the effectiveness of several acupuncture techniques for postoperative pain. The aim of this randomized, controlled trial was to evaluate the efficacy of acupuncture in reducing pain after thyroid surgery.

    METHODS:We randomized 121 patients to a control group (undergoing only standard postoperative analgesic treatment with acetaminophen) and an acupuncture group, undergoing also either electroacupuncture (EA) or traditional acupuncture (TA). Pain was measured according to intraoperative remifentanil use, acetaminophen daily intake, Numeric Rating Scale (NRS), and McGill Pain Questionnaire on postoperative days (POD) 1-3.

    RESULTS:Acupuncture group required less acetaminophen than controls at POD 2 (P = .01) and 3 (P = .016). EA patients required less remifentanil (P = .032) and acetaminophen than controls at POD 2 (P = .004) and 3 (P = .008). EA patients showed a trend toward better NRS and McGill scores from POD 1 to 3 compared with controls. EA patients had a lower remifentanil requirement and better NRS and McGill scores than TA patients. No differences occurred between TA patients and controls.

    CONCLUSION:Acupuncture may be effective in reducing pain after thyroid surgery. EA is more useful; TA achieves no significant effects.

  • The impact of vitamin C on the relationship among inflammation, lipid peroxidation, and platelet activation during analgesic nephropathy in rats.

    Abstract Title:

    The impact of vitamin C on the relationship among inflammation, lipid peroxidation, and platelet activation during analgesic nephropathy in rats.

    Abstract Source:

    J Basic Clin Physiol Pharmacol. 2017 Aug 3. Epub 2017 Aug 3. PMID: 28771433

    Abstract Author(s):

    Nikola Hadzi-Petrushev, Dine Mitrov, Vladimir Kostovski, Mitko Mladenov

    Article Affiliation:

    Nikola Hadzi-Petrushev

    Abstract:

    BACKGROUND:Oxidative stress and inflammation are involved in the pathogenesis of paracetamol-induced renal damage. This study examines the relationship between 8-iso-prostaglandin F2α (8-iso-PGF2α) and platelet activation as well as the relative contribution of the pro-inflammatory markers interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) in enhanced 8-iso-PGF2α biosynthesis, as a complementary onset during analgesic nephropathy induced by chronic treatment with paracetamol. The protective effects of vitamin C on the aforementioned settings are also investigated.

    METHODS:Analgesic nephropathy was induced in Wistar rats. Renal function markers and the activity of antioxidant enzymes were determined spectrophotometrically. Immunoassays were used to measure the pro-inflammatory markers and the markers of lipid peroxidation and platelet activation.

    RESULTS:The chronic treatment with paracetamol led to renal dysfunction, represented by the elevation of plasma urea and creatinine and the decline in the enzymatic antioxidant status, but did not cause a significant increase in TNF-α and IL-1β. The paracetamol-induced lipid peroxidation and enhanced production of 8-iso-PGF2α was not sufficient to cause changes in platelet activation represented by the level of 11-dehydro thromboxane B2.

    CONCLUSIONS:Our results suggest that oxidative stress cannot circumvent the need of stimulation by circulatory cytokines in order to induce inflammatory response and changes in platelet activation during analgesic nephropathy. Vitamin C proved to be beneficial in restoring the renal function markers to normal, increasing the renal enzymatic antioxidant potential, inhibiting lipid peroxidation, and lowering cytokine production and 11-dehydro thromboxane B2 excretion. The observed effects of vitamin C offer support for its potential use as protective treatment in cases of chronic paracetamol overdose.

We use cookies on our website. Some of them are essential for the operation of the site, while others help us to improve this site and the user experience (tracking cookies). You can decide for yourself whether you want to allow cookies or not. Please note that if you reject them, you may not be able to use all the functionalities of the site.