Disease relevance of NSC112930

• Chronic sennoside use induces melanosis coli (MC) and possibly increases colorectal cancer risk [1].
• It is suggested that mitemcinal may be a novel therapeutic agent for constipation that enables easier control of the timing of defecation because of the early onset and short duration of its action, compared with sennoside [2].
• Chronic sennoside treatment does not cause habituation and secondary hyperaldosteronism in rats [3].
• Treatment with the cathartic agent, sennoside, reduced translocation of endotoxin and bacteria, restored intestinal motility, increased mucous secretion, and reduced mortality in a model of acute hemorrhagic pancreatitis in the rat [4].
• The effect of different storage conditions on the chemical stability, laxative effect and acute toxicity of sennoside solutions [5].

High impact information on NSC112930

• Apoptosis induction by sennoside laxatives in man; escape from a protective mechanism during chronic sennoside use [1]?
• To investigate possible mechanisms for carcinogenesis, the effects of acute sennoside use and the presence of MC on colorectal epithelium were studied [1].
• Cytotoxicity of rhein, the active metabolite of sennoside laxatives, is reduced by multidrug resistance-associated protein 1 [6].
• Simultaneously, cell numbers were decreased by DHA-aglycones, but not by sennoside or the biphenylic laxative bisacodyl [7].
• A hybridoma secreting monoclonal antibody against sennoside B was produced by fusing splenocytes from mouse immunized with the sennoside B conjugate and mouse myeloma cells [8].

Biological context of NSC112930

• However, seedlings produced the highest sennoside A + B yield per plant due to the higher leaf biomass [9].
• Metabolic activation of sennoside A in mice [10].
• Except in long term drought, sennoside levels were higher in leaves with lower net photosynthesis, and were increased by treatments that induced physiological stress [9].
• The impact of sennoside-induced intestinal motility and secretory function on bacterial translocation and survival was studied in a rat model of AHP [4].
• The enzyme was optimally active at pH 6.0 for hydrolysis of sennoside B and MUG [11].

Anatomical context of NSC112930

• Large intestine transit time was dose- and time-dependently influenced by sennoside treatment [12].
• In a first histological and ultrastructural study in mouse, we were unable to find any intestinal mucosa injury after long-term sennoside ingestion [13].
• Based on median values, 0.007% of the sennoside intake (calculated as rhein) was excreted in breast milk [14].
• After oral administration, sennoside is degraded only in the lower parts of the gastrointestinal tract, releasing its active metabolite rhein anthrone [15].
• Response to electrical stimulation and acetylcholine was independent of treatment in most segments, but a decrease in maximal contraction was observed by the high daily sennoside dose and by danthron in the ascending colon and descending colon, respectively [16].

Associations of NSC112930 with other chemical compounds

• Effects of drought, foliar nitrogen application and crop type on sennoside yields were studied with simultaneous measurements of net photosynthesis [9].
• Procedures are described for the analysis of the main anthraquinone glycosides of senna powder, senna fruit tablets, and sennoside tablets by high-pressure liquid chromatography (HPLC) [17].
• METHODS: A blinded, experienced colonoscopist examined 132 consecutive patients randomly allocated to receive either a triple regimen consisting of senna syrup (sennoside B), Picolax (sodium picosulphate), and Klean Prep (polyethylene glycol 3350), or Fleet Phospho-soda (sodium dihydrogen phosphate and disodium phosphate dodecahydrate) [18].
• The laxative effect as measured by faecal wet weight during the first 10 h after treatment increased 3- to 4-fold by the higher sennoside doses (daily or intermittently) and 1- to 3-fold by danthron [3].
• Oral administration of senna pod extract dose-dependently (17.5-30 mg kg-1, calculated as sennoside B) reversed net absorption of water, sodium and chloride to net secretion and increased potassium secretion [19].

Gene context of NSC112930

• A sennoside-hydrolyzing beta-glucosidase from Bifidobacterium sp. strain SEN is inducible [20].

Analytical, diagnostic and therapeutic context of NSC112930

• The range of the assay extended from 0.5 ng ml(-1) to 15 ng ml(-1) of sennoside B, and good correlation between ELISA and HPLC methods was obtained when crude extracts of rhubarb were analyzed [8].
• Rapid and simple determination of sennoside A and B in rhei rhizoma by ion-pair high-performance liquid chromatography [21].
• Production of monoclonal antibodies against a major purgative component, sennoside B, their characterization and use in ELISA [8].
• Intracaecal administration reduced time to onset of diarrhoea induced by sennoside C from about 3 h after oral administration to about 24 min [22].
• The low sennoside dose had no measurable effect except on the 1st day (2 fold) compared with the control group [3].

References