Author Oddera S; Silvestri M; Sacco O; Eftimiadi C; Rossi GA Address Division of Pulmonology, G. Gaslini Institute, Genoa, Italy. Source J Lab Clin Med, 124: 2, 1994 Aug, 293-301

Abstract: The processes of phagocytosis and intracellular killing of bacteria by alveolar macrophages (AMs) and polymorphonuclear leukocytes (PMNs) result in the production of reactive oxygen species that can induce self-damage to the phagocytic cells. N-Acetylcysteine (NAC), a mucolytic agent used to treat chronic respiratory inflammatory disorders, possesses antioxidant properties and has therefore been used for the prevention of damage induced by oxygen radicals. This study was designed to evaluate whether NAC can interfere with the processes of phagocytosis and intracellular killing of bacteria and protect the phagocytic cells from self-killing. Human AM, obtained by bronchoalveolar lavage, and peripheral blood PMNs were cultured with Staphylococcus aureus (American Type Culture Collection 25923 strain) in the presence of different concentrations of NAC (1, 10, and 100 mg/L) and two chromophores (4',6'-diamidino-2-phenylindole dihydrochloride and propidium iodide), which identify live or dead bacteria and dead phagocytes. As compared with PMNs, AMs were more effective in ingesting bacteria (p < 0.05) and were equally effective as intracellular killers (p > 0.05), but were susceptible to a significantly higher rate of self-killing (p < 0.01). The presence of NAC in the cell cultures at the highest dose tested (100 mg/L) induced a significant enhancement of the bactericidal activity of both AMs (p < 0.05) and PMNs (p < 0.05). This increased intracellular killing was not associated with increased proportions of dead phagocytes either in AMs or PMNs cultures (p > 0.05, each comparison), suggesting a protective effect of NAC on damage induced by toxic products generated during phagocytosis.

Title N-acetylcysteine inhibits muscle fatigue in humans. Author Reid MB; Stokic DS; Koch SM; Khawli FA; Leis AA Address Department of Medicine, Baylor College of Medicine, Houston, Texas 77030. Source J Clin Invest, 94: 6, 1994 Dec, 2468-74

Abstract: N-acetylcysteine (NAC) is a non specific antioxidant that selectively inhibits acute fatigue of rodent skeletal muscle stimulated at low (but not high) tetanic frequencies and that decreases contractile function of unfatigued muscle in a dose-dependent manner. The present experiments test the hypothesis that NAC pretreatment can inhibit acute muscular fatigue in humans. Healthy volunteers were studied on two occasions each. Subjects were pretreated with NAC 150 mg/kg or 5% dextrose in water by intravenous infusion. The subject then sat in a chair with surface electrodes positioned over the motor point of tibialis anterior, an ankle dorsiflexor of mixed-fiber composition. The muscle was stimulated to contract electrically (40-55 mA, 0.2-ms pulses) and force production was measured. Function of the unfatigued muscle was assessed by measuring the forces produced during maximal voluntary contractions (MVC) of ankle dorsiflexor muscle groups and during electrical stimulation of tibialis anterior at 1, 10, 20, 40, 80, and 120 Hz (protocol 1). Fatigue was produced using repetitive tetanic stimulations at 10 Hz (protocol 1) or 40 Hz (protocol 2); intermittent stimulations subsequently were used to monitor recovery from fatigue. The contralateral leg then was studied using the same protocol. Pretreatment with NAC did not alter the function of unfatigued muscle; MVC performance and the force-frequency relationship of tibialis anterior were unchanged. During fatiguing contractions stimulated at 10 Hz, NAC increased force output by approximately 15% (P < 0.0001), an effect that was evident after 3 min of repetitive contraction (P < 0.0125) and persisted throughout the 30-min protocol. NAC had no effect on fatigue induced using 40 Hz stimuli or on recovery from fatigue. N-acetylcysteine pretreatment can improve performance of human limb muscle during fatiguing exercise, suggesting that oxidative stress plays a causal role in the fatigue process and identifying antioxidant therapy as a novel intervention that may be useful clinically.

Title [Omeprazole/amoxicillin: improved eradication of Helicobacter pylori in

smokers because of N-acetylcysteine] Original Title Omeprazol/Amoxicillin: verbesserte Eradikation von Helicobacter pylori bei Rauchern durch N-Acetylcystein. Author Zala G; Flury R; W=FCst J; Meyenberger C; Ammann R; Wirth HP Address

Departement f=FCr Innere Medizin, Universit=E4tsspital Z=FCrich. Source Schweiz Med Wochenschr, 124: 31-32, 1994 Aug 9, 1391-7

Abstract Colonization of Helicobacter pylori (HP) beneath the protective film of gastric mucus enables the organism to survive in the hostile environment of the gastric mucosa. N-acetylcysteine (NAC), a sulfhydryl compound with potent mucolytic activity, induces a reduction of gastric barrier mucus thickness of about 75% and reduces mucus viscoelasticity. We therefore tested the hypothesis whether better eradication results could be achieved by addition of NAC to omeprazole/amoxicillin (OME/AMOX). 34 HP positive outpatients with endoscopically documented recurrent duodenal ulcer were included in an ongoing, prospective, randomized trial. Exclusion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids or NSAIDs within 4 weeks before study entry. Patients currently smoking > 10 cigarettes/day were classified as smokers. HP infection was confirmed by histology (3 biopsy specimens from gastric antrum and 2 from gastric body; H&E, Giemsa) and at least positive rapid urease test or culture. All 34 patients underwent ulcer therapy with OME (20 mg per day) for 20 days (d 1-20). Group A: in 17 patients (5 females, 12 males, mean age 46 [29-74] years; 8 smokers, 9 nonsmokers) the subsequent eradication therapy, consisting of oral OME (40 mg bid) and AMOX solute (750 mg tid) for 10 days, was combined with NAC solute (2 x 600 mg bid (d 21-30). Group B: 17 patients (2 females, 15 males, mean age 39 [19-70] years; 11 smokers, 6 nonsmokers) underwent eradication therapy without NAC (d 21-30). Control endoscopy was done after a minimal interval of 30 days from the end of treatment.

Also make sure to read these books: Poison in Your Teeth: Mercury Amalgam (Silver) Fillings...Hazardous to Your Health! and Mercury Detoxification by Tom McGuire