The influence of harvest time on total phenolic and flavonoid contents, antioxidant, antibacterial and cytotoxicity of Rheum khorasanicum root extract.

INTRODUCTION: For many centuries, medicinal herbs and their derivatives have been used to treat or prevent various diseases. However, environmental factors such as the season for collection of plant may change the therapeutic efficacy. The present work investigates seasonal variations of phenolic, flavonoid content, antioxidant, antibacterial, and cytotoxic potential of hydroalcoholic extract of Rheum khorasanicum (HER). METHODS: R. khorasanicum was collected in three different months: December, February, and April. The Folin-Ciocalteu assay was applied to measure the total phenolic content of HER. Antioxidant activities (DPPH and FRAP) were also determined. Next, the extracts were evaluated for antibacterial potential against some Gram-positive and Gram-negative strains. The minimal inhibitory concentration (MIC) was determined by the microdilution method. Finally, the effect of extracts on the viability of C6, A549, and HT-29 cells was evaluated via the MTT assay. RESULTS: All three extracts contained considerable phenolic and flavonoid contents and showed desirable antioxidant activity. The April sample exhibited the greatest phenolic and flavonoid content and significant antioxidant activity potential in the FRAP test. In addition, the April sample had the highest antibacterial activity and cytotoxic effect on the cancerous cell lines. CONCLUSION: The April extract showed more antioxidant, antibacterial and cytotoxic effect, probably because of its higher phenolic and flavonoid contents than other samples. These results demonstrate that the harvest timing of R. khorasanicum affects the plant's phenolic content and its antioxidant and cytotoxicity activities.

A rare ganglioneuroblastoma secreting dopamine and the value of its measurement in diagnosis and prognosis.

A case is described of a patient with a ganglioneuroblastoma, initially located in the right adrenal, which produced an excess of dopamine (7646 and 7959 nmol/24 h), approximately two and a half times the upper limit of the normal daily urine output. The urinary excretion of noradrenaline, adrenaline and methylated derivatives was always within the normal reference ranges. The patient was generally well, with normal blood pressure and only mild flushes. Two years after surgical resection, recurrence was indicated by an increase in urinary dopamine (8507 nmol/24 h); it was located in the tumour bed and left side of the neck by CT and (123)I MIBG scans. The patient was treated with a high dose of (131)I MIBG, with subsequent reduction in dopamine production. This was repeated on four other occasions, the latest being in January 2005. The output of dopamine was thus used as a marker of tumour diagnosis and progression and it is recommended that the assay of dopamine be included in the screening of catecholamine-secreting tumours to avoid possible misdiagnosis.

In-vitro studies of aluminium-induced toxicity on kidney proximal tubular cells.

The toxicity of aluminium (Al) to various cells is well described. However, little is known about its effect on kidney cells, which can be exposed to relatively high concentrations. In this study, the effect of aluminium as the citrate complex in concentrations up to 100 microM/l was investigated using a monolayer cell culture of kidney proximal tubular cells (PTC). Aluminium was found to be slightly toxic; at 100 microM/l the PTCs lost viability by 15, 20 and 24% after incubation for 24, 48 and 72 h, respectively. Viability was significantly reduced (P<0.001) after 48 h incubation with aluminium concentrations of 25, 50, 75 and 100 microM/l compared with controls. Lactate dehydrogenase (LDH) release was significantly increased (P<0.001) with 100 microM/l Al to 44.67+/-1.76 and 50.33+/-0.88 compared with controls 24+/-1.00 and 28.33 2.34 U/l after 24 and 48 h incubation, respectively, indicating damage to the plasma membrane. However, N-acetyl-beta-D-glucosaminidase (NAG) release in the medium of cells exposed to aluminium showed no difference from control values (P>0.1). Glucose consumption in aluminium-exposed cells at 100 microM/l was slightly, but not significantly (P=0.14), increased during 48 h incubation. Electron micrographs of cells exposed to aluminium at 100 microM/l showed a slight reduction in microvilli density and the cell tight junctions were not as clear compared with the control cells. Pretreatment with protective agents glutathione and tiopronin partly restored the viability of kidney proximal tubular cells to control values, whereas vitamin C and/or cysteine showed no effect. This study indicates that aluminium may show toxicity to kidney cells in culture. Several sites on the cell, i.e. microvilli, membrane and the cell junction, seem to be affected, however the mechanism(s) of damage remain unclear.