Emodin Concentration Research Articles

Within population variation and interrelationships between morphology, nutritional content, and secondary compounds of Rhamnus alaternus fruits.

• We studied within-species variation in and interrelations among morphological and chemical traits of ripe Mediterranean buckthorn ( Rhamnus alaternus ) fruit, a bird-dispersed species. • Principal component analysis revealed that larger fruits tended to be relatively rich in nonstructural carbohydrates (NSC), water and P but poor in protein and most minerals. Small fruits tended to be relatively rich in protein, structural carbohydrates, K and Zn while intermediate size fruits tended to be rich in lipids, Mg and Ca. Variation in chemical traits (organic compounds and minerals) was typically much higher than in morphological traits (e.g. fruit size) with the exception of NSC and water content, which varied little. This discrepancy might be explained by differences in environmental conditions between plant microsites that imposed greater variability on fruit nutrient composition than on fruit-morphological traits; and by lower selective pressure by birds on fruit chemical traits than on morphological traits. • Secondary metabolite (emodin) concentration was positively correlated with concentrations of NSC, supporting the nutrient/toxin titration model, which predicts that high levels of secondary metabolites in fruits should be off set by high nutritional rewards for dispersers. • Emodin concentration in leaves was much higher than in fruit pulp, which may indicate its differential adaptive roles in seed dispersal and against herbivores.

A novel function of emodin: Enhancement of the nucleotide excision repair of UV- and cisplatin-induced DNA damage in human cells

Nucleotide excision repair (NER) is the main pathway by which mammalian cells remove carcinogenic DNA lesions caused by UV light and many other common mutagens. To explore the effect of emodin on NER, its influence on the repair of UV- and cisplatin-induced DNA damage in human fibroblast cells (WI38) was evaluated. Emodin increased unscheduled DNA synthesis (UDS) of UV-treated cells and reduced cisplatin-induced DNA adducts in WI38 in a concentration-dependent manner, indicating that emodin might promote NER capability in cells. The resultant NER complex is a cooperative assembly of XPF, ERCC1, XPA, RPA, and XPG subunits. The gene regulations of the subunits after emodin treatment were determined by reverse transcription-polymerase chain reaction (RT-PCR) using specific primers. Among the subunits, the expression of ERCC1 in WI38 cells was up-regulated significantly after emodin treatment. All other expressions remained essentially unchanged. In addition, calcium influx in WI38 was increased in proportion to the concentration of emodin. Since UV-induced NER is Ca 2+ dependent, elevation of calcium influx may be another mechanism by which emodin facilitates DNA repair. In conclusion, emodin can increase the repair of UV- and cisplatin-induced DNA damage in human cells, and elevated ERCC1 gene expression and Ca 2+-mediated DNA repair processes may be involved in the repair mechanism of emodin.

دراسات كهروكيماوية على مركب الايمودين بطريقة الانتزاع الكاثودي الامتصاصي

A differential pulse cathodic stripping voltammetric (DP-CSV) method for determination of emodin in Britton- Robinson buffer (pH2) at a hanging mercury drop electrode (HMIDE) is described. The method is based on measuring the reductive peak height at —0.25V vs. Ag/AgCl reference electrode. The linear relationship between the peak current and emodin concentration allowed the voltarnmetric determination of emodin over a wide concentration range 1.0 X 10-2 —2.5 X10-6 M, with a relative standard deviation of 3.3% (10 determinations at 1 X 10-2 M). Adsorption of emodin at HMDE enabled a detection limit of 2X10-1°M after 3 min accumulation at 0.0V. The applicability of the suggested method was found to be suitable for the determination of emodin in roots, stems and leaves of Rumex cyprius plant.

Emodin-induced inhibition of growth and DNA damage in the Helicobacter pylori.

Studies were conducted to examine the dose effects of emodin on inhibition of growth versus DNA damage events in H. pylori from patients who had peptic ulcer disease. Inhibition of growth study from H. pylori demonstrated that emodin elicited dose-dependent growth inhibition in H. pylori cultures; that is, the greater the concentration of emodin, the greater the growth inhibition to H. pylori. However, S1 nuclease sensitivity analysis studies revealed that emodin induced dose-dependent DNA damage in H. pylori. Collectively, these results suggest that there was a possible relationship between the dose response to emodin and the inhibition of growth and DNA damage in H. pylori.