[Drug or plant substances which antagonize venoms or potentiate antivenins] Paraquat-induced free radical reaction in mouse brain microsomes. Central effects of the H1-antihistamine, cetirizine. Rx drugs

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Bull Soc Pathol Exot. 1997;90(4):282-5.
[Drug or plant substances which antagonize venoms or potentiate antivenins]

[Article in French]

Chippaux JP, Rakotonirina VS, Rakotonirina A, Dzikouk G.

Antenne ORSTOM aupres du Centre Pasteur du Cameroun, Adresse actuelle, Niamey, Niger.

Dendroaspis jamesoni (Elapidae) and Echis oceliatus (Viperidae) are responsible for most of severe evenomation in Cameroon. Toxicity of venoms of these two species has been measured using mice according to the method of Spearman & Karber. The effect on experimental envenomation of various drugs (atropine, promethazine, neostigmine, hydrocortisone, pentosane sulfuric polyester, heparin, tranexamic acid and aminocaproic acid) and plant extracts (Schumanniophyton magnificum, Bidens pilosa, Securidaca longepedunculata and Garcinia lucida) has been observed associated or not with the antivenom lpser Afrique (SAV). The venom of D. jamesoni contains neurotoxins agonizing and antagonising acetylcholine. The toxicity of the venom did not depend on the route of injection. Atropine, promethazine, neostigmine and hydrocortisone protected animals against a venom dose up to 2 LD50. Moreover, atropine and promethazine potentiated the SAV. Similar results have been obtained with extracts from S. magnificum and B. pilosa. The venom of E. ocellatus induces haemorrhage and necrosis. The toxicity increased by 3-fold when the venom was injected through intravenous or intraperitoneal route, compared to intramuscular route. Pentosane sulfuric polyester and tranexamic acid protected mice against doses up to 3 LD50. Pentosane sulfuric polyester, hydrocortisone, heparin and aminocaproic acid increased the SAV protective titre by 50%. However, tried plant extracts weakly antagonised the venom and did not potentiate the SAV.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9479470&dopt=Abstract

Neurochem Res. 1998 Jan;23(1):47-53.
Paraquat-induced free radical reaction in mouse brain microsomes.

Yang W, Sun AY.

Department of Pharmacology, University of Missouri, Columbia 65212, USA.

Paraquat has been implicated as an environmental toxin which may induce the syndrome of Parkinson's disease after exposure to this agent. However, the biochemical mechanism by which paraquat causes cell death and neurodegeneration has not been extensively studied. Paraquat was rapidly taken up by nerve terminals isolated from mouse cerebral cortices. It induced lipid peroxidation in a concentration dependent manner in the presence of NADPH and ferrous ion. The maximal stimulation effect was obtained at a paraquat concentration around 100 microM and the Km value for paraquat was 46.7 microM. The lipid peroxidation required microsomal enzymes. Antioxidants, such as superoxide dismutase, catalase and promethazine significantly inhibited paraquat-induced lipid peroxidation. Due to its structural similarity to the pyridinium compound MPP+ (N-methyl-4-phenyl pyridium ion), it may be taken up by dopamine neurons and cause lipid peroxidation and cell death resulting in the manifestation of Parkinsonian syndrome.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9482266&dopt=Abstract

Aviat Space Environ Med. 1998 Feb;69(2):166-71.
Central effects of the H1-antihistamine, cetirizine.

Nicholson AN, Turner C.

Royal Air Force School of Aviation Medicine, Farnborough, Hampshire, United Kingdom.

BACKGROUND: Effects of the H1-antihistamine, cetirizine, were studied on daytime alertness and performance to establish whether the drug would be suitable for use by air personnel and others involved in skilled activity. METHODS: The investigation was carried out in six healthy volunteers, and the effects of the drug (5, 10, and 15 mg) were studied on sleep latency, subjective sleepiness, digit symbol substitution, tracking and vigilance from 0.5 h to 7.5 h after ingestion. The study was placebo-controlled and double-blind with a six-way cross-over design. Promethazine (10 mg) was used as an active control to establish the sensitivity of the experimental procedures. RESULTS: Promethazine (10 mg) decreased the mean level of vigilance over the day, increased objective and subjective sleepiness from 1.5 to 5.5 h, and impaired tracking 5.5 h after ingestion. Cetirizine (10 and 15 mg) led to shortened sleep latencies over the day, and at 7.5 h sleep latencies were shorter with 10 mg cetirizine than with placebo. Subjective sleepiness with cetirizine was increased compared with placebo after 5 mg at 1.5 h, 10 mg at 7.5 h, and 15 mg at 5.5 h and when meaned over the day. Tracking was impaired with 5 and 15 mg cetirizine 0.5 h after ingestion. CONCLUSION: The study failed to establish dose-response effects of cetirizine, but it is evident that cetirizine is not free of central activity over the therapeutic range, and so its use by air personnel is not recommended.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9491258&dopt=Abstract

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