Oxalated, Sulphated and Primary Glycosides

Fairbairn, James

doi:10.1159/000137402

Cited by 3 publications

(3 citation statements)

References 9 publications

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“…It is present in aloe-vera leaves [3,4]. It is believed to be a good inhibitor for the proliforation of different types of cancers [4][5][6] without any damage to the normal cells [7][8][9][10]. It shows toxicity for malignant tumor such as neuroblastoma cells, Ewing's sarcoma cells etc.…”

Section: Introductionmentioning

confidence: 99%

Significance of Species Sensitive Electrochemical Methods for the Analysis of Antineuractodermal Agent AE (Aloe-Emodin)

Modi¹,

Pitre²

2010

Reviews in Analytical Chemistry

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Species sensitive Direct current (DCP) and differential pulse polarographic (DPP) methods have been developed and authenticated for the qualitative as well as quantitative analysis of antineuractodermal agent, Aloe-Emodin (AE) in natural origin, human blood sample and industrial samples. 10 mm AE produces a well defined polarographic reduction wave/peak in acetate buffer with Ε'Λ/Ερ = -1140 mv Vs SCE at pH 6.5 + 0.1, however, the EVil Ep value shifts to more electronegative value with increase in AE concentration due to change of the viscosity of the medium. The developed electrochemical methods have been standardized for the analysis of Aloe-Emodin (Antineuroactodermal agent) in pharmaceutical formulations. The electrochemical analysis has been supplemented by FTIR spectroscopic and HPLC methods. An isocratic high performance liquid chromatography (HPLC) method has also been developed and validated to determine AE in human blood plasma. The HPLC separation was carried out on symmetry shield RP18 a mobile phase of methanol -water-acetic acid (65:35:02) and UV detection of λβχ = 410 nm and Xem = 510 nm. The retention time of AE was 4.25 min.

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Section: Introductionmentioning

confidence: 99%

Significance of Species Sensitive Electrochemical Methods for the Analysis of Antineuractodermal Agent AE (Aloe-Emodin)

Modi¹,

Pitre²

2010

Reviews in Analytical Chemistry

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“…The crude senna drug, for instance, has been found to be 1.7 times as active as pure sennosides (Fairbairn & Moss 1970;Fairbairn 1980). The crude senna drug, for instance, has been found to be 1.7 times as active as pure sennosides (Fairbairn & Moss 1970;Fairbairn 1980).…”

mentioning

confidence: 99%

“…Studies on the laxative effect of senna products have shown it to be even higher than expected on the basis of the chemically measured content of sennosides. The crude senna drug, for instance, has been found to be 1.7 times as active as pure sennosides (Fairbairn & Moss 1970;Fairbairn 1980). Thus the decomposition products or other constituents may also have a laxative effect, providing misleading evidence as to the stability of the liquid senna products.…”

mentioning

confidence: 99%

The Effect of Different Storage Conditions on the Chemical Stability, Laxative Effect and Acute Toxicity of Sennoside Solutions

Lainonen¹,

Marvola²,

Hietala³

et al. 1988

Pharmacology & Toxicology

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This paper investigates the effect of different storage conditions on the chemical stability, laxative effect and acute toxicity of sennoside solutions. The variables in storage conditions were pH, time and temperature (room temperature or 100 degrees). The chemical stability of sennosides in aqueous solutions was found to be pH-dependent, with the best stability at pH 6.5 (t90. = 8.4 months) and the poorest at pH 8.0 (t90. = 2.5 months). Two years of storage at room temperature did not reduce the laxative potency in mice, regardless of the pH. After 4.25 years of storage the potency declined in alkaline solutions only. The degradation products with laxative potencies are chemically unknown. The acute toxicity of sennoside solutions increased with time during storage, the acid solution being more toxic than either the neutral or alkaline ones.

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Mechanism of arginine-stimulated Ca2+ influx into pancreatic B cell

Herchuelz¹,

Lebrun²,

Boschero³

et al. 1984

American Journal of Physiology-Endocrinology and Metabolism

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The mechanism by which arginine stimulates Ca2+ inflow into the pancreatic B cell was investigated. Arginine (10 mM) increased 86Rb outflow from perifused rat pancreatic islets, suggesting that arginine-stimulated Ca2+ influx into the B cell does not result from a decrease in K+ conductance. Arginine stimulated Ca2+ uptake in isolated islets over short incubation periods and increased 45Ca outflow from perifused islets in a Ca2+-dependent manner. The calcium channel blocker verapamil inhibited both arginine-stimulated 45Ca uptake and 45Ca outflow. However, the sensitivity toward verapamil of arginine-stimulated islets was lower than that of islets stimulated by 20 mM K+, which gates voltage-sensitive Ca2+ channels. It was similar to that of islets stimulated by 8.3 mM glucose, which is thought to mainly gate voltage-insensitive Ca2+ channels. It is suggested that arginine stimulates Ca2+ inflow into the B cell by gating voltage-insensitive Ca2+ channels. The arginine-induced stimulation of Ca2+ inflow could participate in the depolarizing action of the amino acid on the B cell membrane.

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Oxalated, Sulphated and Primary Glycosides

Cited by 3 publications

References 9 publications

Significance of Species Sensitive Electrochemical Methods for the Analysis of Antineuractodermal Agent AE (Aloe-Emodin)

Significance of Species Sensitive Electrochemical Methods for the Analysis of Antineuractodermal Agent AE (Aloe-Emodin)

The Effect of Different Storage Conditions on the Chemical Stability, Laxative Effect and Acute Toxicity of Sennoside Solutions

Mechanism of arginine-stimulated Ca2+ influx into pancreatic B cell

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