Rauwolfia serpentina
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References
Awang DV, Dawson BA, Neville GA, Ekiel I, Deslauriers R, Smith IC. 13C-NMR of Rauwolfia alkaloids.
J Pharm Biomed Anal. 1990;8(1):91.
Bhatara VS, Gupta S. History of Rauwolfia serpentina. Can J Psychiatry. 1997 Sep;42(7):777-778. (Letter)
Bhatara VS, Sharma JN, Gupta S, Gupta YK. Images in psychiatry. Rauwolfia serpentina: the first herbal
antipsychotic. Am J Psychiatry. 1997 Jul;154(7):894.
Brinker F. The Toxicology of Botanical Medicines. Revised second ed. Sandy, Oregon: Eclectic Medical Publications, 1996.
Cieri UR. Determination of reserpine and rescinnamine in Rauwolfia serpentina powders and tablets: collaborative study.
J AOAC Int. 1998 Mar-Apr;81(2):373-380.
Abstract: A liquid chromatographic (LC) method for determining reserpine and rescinnamine in Rauwolfia serpentine powders and tablets, which uses fluorescence detection, was subjected to a collaborative study. The procedure for extraction and purification is a simplified version of that used in the current official method for analysis of these products. LC separations are performed on a normal-phase column. The mobile phase is methanol to which a small volume of an aqueous solution of 1-pentanesulfonic acid sodium salt can be added to achieve desired elution characteristics. Reserpine and rescinnamine elute at approximately the same time but can be individually quantitated by appropriate settings of the fluorescence detector. Reserpine is determined at an excitation wavelength of 280 nm and an emission wavelength of 360 nm, because rescinnamine is completely non-fluorescent at these wavelengths. Rescinnamine is determined at an excitation wavelength of 330 nm and an emission wavelength of 435 nm, because reserpine is completely nonfluorescent at these wavelengths. The following materials were used for the study: one sample of United States Pharmacopeia (USP) standard R. serpentine powder, one tablet type labeled as containing 100 mg R. serpentine and 2 tablet types labeled as containing 50 mg R. serpentine. For each of the 4 materials, 2 pairs of blind duplicates were prepared. Three materials were analyzed in duplicate by 8 laboratories. One of the 2 tablets labeled to contain 50 mg R. serpentine was analyzed only by 7 of 8 participating laboratories. Average combined content of reserpine and rescinnamine was 0.144% for the USP raw material and 0.132, 0.135, and 0.137% for the 3 commercial tablets. Reproducibility relative standard deviation values were 5.72, 5.93, 8.61, and 3.48% and repeatability relative standard deviation values were 2.57, 4.87, 3.19, and 1.99% for the 4 samples. The Associate Referee conducted a study to determine recoveries of reserpine plus rescinnamine by this method from mixtures simulating sample extracts. Average recovery of 15 determinations was 100.1%, with a relative standard deviation of 1.3%. The LC method for determination of reserpine and rescinnamine in R. serpentine powders and tablets has been adopted first action by AOAC INTERNATIONAL.
Dreisbach RH. Handbook of Poisoning: Prevention, Diagnosis, and Treatment. Tenth ed. Grand Rapids, MI: Lange Medical Publications, 1980.
Duke JA. CRC Handbook of Medicinal Herbs Boca Raton, FL. CRC Press, 1985.
Fujimiya M, Okumiya K, Nakazawa M, Kitahama K, Kimura H, Maeda T. Effect of reserpine on 5-hydroxytryptophan (5HTP)-immunoreactive neurons in the rat brain.
Histochemistry. 1994 Jan;101(1):21-26.
Abstract: By immunohistochemistry of rat brain in conjunction with a specific antibody against 5-hydroxytryptophan (5HTP), we examined immunoreactivity to 5HTP in neurons, from which 5-hydroxytryptamine (5HT; serotonin) was depleted by reserpine treatment. The distribution patterns of 5HTP-positive neurons overlapped with those of 5HT neurons. Treatment with reserpine (5 mg/kg, 90 min before death) caused a complete suppression of 5HT-positive staining, but 5HTP-immunostaining remained in perikarya of the nuclei raphe dorsalis, centralis superior and obscurus. Treatment with reserpine (25 mg/kg, 90 min before death) suppressed the 5HTP-immunoreaction in certain perikarya (e.g. of the nucleus raphe dorsalis) and fibres; however, 5HTP-immunostaining remained in perikarya of the nuclei centralis superior and raphe obscurus. This suggests that these neurons synthesize more 5HTP by a process which appears to be stimulated by reserpine.
Hardman J, et al. (eds.) Goodman & Gilman's Pharmacological Basis of Therapeutics.
Ninth Edition. McGraw Hill, 1996.
Henriques JA, Moreno PR, Von Poser GL, Querol CC, Henriques AT. Genotoxic effect of alkaloids. Mem Inst Oswaldo Cruz. 1991;86 Suppl 2:71-74.
Keeler RF, Tu AT. Handbook of Natural Toxins. New York: Marcel Dekker, Inc., 1983.
Langer P, Greer MA. Anti-Thyroid Substances and Naturally Occurring
Goitrogens. New York: Karyer, Greer, 1977.
Schmauss M, Erfurth A. [Combination therapies in antidepressive drug refractory depression--an overview].
Fortschr Neurol Psychiatr 1996 Oct;64(10):390-402. [Article in German]
Abstract: Despite the availability of a wide range of effective antidepressant drugs, nearly 30% of depressed patients fail to respond to antidepressant treatment. Various pharmacological strategies have been developed to treat such refractory depression, of which augmentation therapies are one of the most important. This article reviews both benefits and risks of all known augmentation therapies. Among these treatment strategies the efficacy of lithium augmentation is very well documented by a large number of controlled studies - lithium augmentation can therefore be recommended in depression refractory to antidepressant treatment. The efficacy of triiodothyronine (T3) augmentation and the combination of different antidepressants - like a TCA-MAOI combination - is described in a large number of case reports and uncontrolled studies; the number of placebo controlled double blind studies, confirming the efficacy of these treatment strategies, is however relatively small. T3 augmentation and combined antidepressant treatment may therefore be considered in the treatment of refractory depression; in contrast to lithium augmentation these combination therapies are however only second-line strategies. Other augmentation therapies (TCA + stimulants, TCA + reserpine, TCA + yohimbine, TCA + fenfluramine, SSRI + buspirone) are very interesting clinical research strategies, but don't have too much importance in clinical practice at the moment.
Simpson LL, Curtis DR. Neuropoisons; Their Pathophysiological Actions. New York: Plenum Press, 1997.
Stanford JL, Martin EJ, Brinton LA, Hoover RN. Rauwolfia use and breast cancer: a case-control study.
J Natl Cancer Inst. 1986 May;76(5):817-22.
Abstract: Breast cancer risk among 1,362 cases and 1,250 controls participating in a large multicenter screening program was examined in relation to hypertension and the use of rauwolfia derivatives. A previous diagnosis of hypertension, reported by 22% of the cases and 23% of the controls, was not associated with an increased risk of breast cancer [odds ratio (OR) = 0.9]; nor was there any excess risk for long-term hypertensives. In addition, there was no significant increase in risk associated with use of either rauwolfia derivatives (OR = 1.2), thiazide preparations (OR = 1.2), or methyldopa (OR = 1.1). However, there were significant excess risks among long-term users and those with extended intervals since first use of rauwolfia. Rauwolfia users of 10 or more years' duration or those whose initial use occurred greater than or equal to 10 years before diagnosis had risk ratios of 4.5 (95% Cl, 1.2-19.8) and 3.8 (95% Cl, 2.3-11.6), respectively. These results suggest that women exposed to long-term rauwolfia use have an elevated risk of developing breast cancer, although the results fail to support previous observations of a generalized adverse effect.
Thien T, Benneker JC. [Alternative medication not always harmless]. Ned Tijdschr
Geneeskd. 1994 Feb 5;138(6):315. [Article in Dutch]
Thienes CH, Haley TJ. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1975.
Tona L, Kambu K, Mesia K, Cimanga K, Apers S, De Bruyne T, Pieters L, Totte J, Vlietinck AJ. Biological screening of traditional preparations from some medicinal plants used as antidiarrhoeal in Kinshasa, Congo.
Phytomedicine. 1999 Mar;6(1):59-66.
von Poser G, Andrade HH, da Silva KV, Henriques AT, Henriques JA. Genotoxic, mutagenic and recombinogenic effects of rauwolfia alkaloids.
Mutat Res. 1990 Sep;232(1):37-43.
Abstract: In the last decade, the possible correlation between the use of reserpine and rauwolfia drugs as antihypertensive agents and breast cancer incidence has been investigated. For the purpose of evaluating the mutagenic and genotoxic effects of these drugs, reserpine and ajmalicine were studied using the SOS Chromotest and the induction of gene conversion, crossing-over and reverse mutation in the yeast diploid strain XS2316. The results indicated a lack of genotoxic, mutagenic and recombinogenic effects.
von Oettingen WF. Poisoning: A Guide to Clinical Diagnosis and Treatment. Philadelphia: W.B. Saunders and Company, 1958.
Warzecha H, Obitz P, Stockigt J. Purification, partial amino acid sequence and structure of the product of raucaffricine-O-beta-D-glucosidase from plant cell cultures of Rauwolfia
serpentina. Phytochemistry. 1999 Apr;50(7):1099-1109.
Abstract: Plant cell suspension cultures of Rauwolfia produce within 1 week approximately 250 nkat/l of raucaffricine-O-beta-D-glucosidase. A five step procedure using anion exchange chromatography, chromatography on hydroxylapatite, gel filtration and FPLC-chromatography on Mono Q and Mono P delivered in a yield of 0.9% approximately 1200-fold enriched glucosidase. A short protocol employing DEAE sepharose, TSK 55 S gel chromatography and purification on Mono Q gave a 5% recovery of glucosidase which was 340-fold enriched. SDS-PAGE showed a Mr for the enzyme of 61 kDa. The enzyme is not glycosylated. Structural investigation of the enzyme product, vomilenine, demonstrated that the alkaloid exists in aqueous solutions in an equilibrium of 21(R)- and 21(S)-vomilenine in a ratio of 3.4:1. Proteolysis of the pure enzyme with endoproteinase Lys C revealed six peptide fragments with 6-24 amino acids which were sequenced. The two largest fragments showed sequences, of which the motif Val-Thr-Glu-Asn-Gly is typical for beta-glucosidases. Sequence alignment of these fragments demonstrated high homologies to linamarase from Manihot esculenta (81% identity) or to beta-glucosidase from Prunus avium (79% identity). Raucaffricine-O-beta-D-glucosidase seems to be a new member of the family 1 of glycosyl hydrolases.
Weiss RF. Herbal Medicine. Beaconsfield, England: Beaconsfield Publishers Ltd., 1988.
Woodson RE Jr, Youngken HW, Schittler E, Schneider JA. Rauwolfia: Botany, Pharmacognosy, Chemistry, and Pharmacology. Boston: Little, Brown, and Company, 1957.