[Measuring the lead, arsenic, copper, zinc, selenium, sodium, potassium, nickel, and magnesium ions in black tea]

Background: high intake of some elements results in toxicity for human. Investigations has been shown that in some species of tea [Camellia sinensis L] the level of certain elements are higher than standard. This study aimed to measure the amount of K, Cu, Pb, Ni, Na, Mg, Zn, Ar, and Se ions in black tea

Matereials and Methods: pre-analysis treatment of tea samples [trademarks Tala, Gulabi, Ahmad, Golestan, and the bulk brand of Ceylon] and the measurement of ions were carried out using acid digestion and atomic-absorption spectrometry techniques, respectively

Results: the minimum and maximum means for K, Mg, Zn, Cu, Pb, Ni, and Na ions in the examined samples were [18062 +/- 1095 and 19364 +/- 6120 mg/kg], [1 +/- 0 and 157 +/- 20 mg/kg], [21 +/- 3 and 31 +/- 9 mg/kg], [17 +/- 0 and 21 +/- 0 mg/kg], [0.485 +/- 0.249 and 0.151 +/- 0.066 mg/kg], [0.485 +/- 0.249 and 0.151 +/- 0.066 mg/kg], [2.907 +/- 0.077 and 6.987 +/- 1.270 mg/kg], [1 +/- 0 and 157 +/- 20 mg/kg], respectively. Se and Ar levels is samples were non-detectable

Conclusion: the availability of high levels of K and Mg ions in the examined black teas is in agreement with a traditional medicine hypothesis signifying the use of tea to decrease the blood pressure

Molecular basis of G6PD deficiency: Current status and its perspective

Glucose-6-phosphate dehydrogenase is an essential enzyme to cell growth. Its deficiency of enzyme plays an important role in senescence and death signaling. Also, it is actually the most common clinically important enzyme defect, not only in hematology, but also among all human known diseases. Clinical consequences of enzyme deficiency are: neonatal hyperbilirubinemia, acute hemolytic anemia, and chronic hemolytic anemia. The enzyme gene spans 18 kb on the X chromosome [xq28] and contains 13 exons. Its promoter is embedded in a CpG island that is conserved from mice to humans. The development of a number of PCR-based methods for the detection of known mutations in Glucose- 6-phosphate dehydrogenase has made it possible to detect enzyme deficiency and identify the specific mutation responsible with relative ease. We will discuss the mentioned clinical manifestations of glucose-6-phosphate dehydrogenase deficiency, Genetics, biochemistry and pathophysiology of the enzyme in details using newer published data and present most of the studies in Iranian population