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One of the main reasons for conducting toxicology studies is to determine the risk or in other words to determine the potential for harm towards human health or the environment upon exposure to naturally occurring or synthetic agents. Thus the findings of this study will hopefully contribute to a better understanding in predicting Best Place To Buy Kratom Leaf the risk upon consuming Mitragyna speciosa Korth leaves. M human consumption Best Place To Buy Kratom Leaf of Mitragyna speciosa Korth leaves at pharmacologically active doses would appear to be substantially lower than the threshold of toxicity predicted from my in vitro study. Taking into account all the findings of my studies MSE and MIT could be potentially harmful in humans at high doses. The safety assessment assumptions suggest that the use of Mitragyna speciosa Korth leaves within the range of pharmacologically active doses as reported in the literature is probably safe however caution should be taken as MSE toxicity in this study was found kratom for drug addiction to be enhanced by metabolism particularly by CYP 2E1. Thus the combination consumption of Mitragyna speciosa Korth leaves with CYP Best Place To Buy Kratom Leaf 2E1 inducers may shift toxicity closer to doses that are pharmacologically active. Based on the current findings observed in the present studies it is concluded that the methanol-chloroform extract (MSE) of the Mitragyna speciosa Korth (Kratom) leaves and its dominant alkaloid mitragynine (MIT) have potential to cause cytotoxicity to mammalian cells at high doses and is possibly harmful to human users.
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This phenomenon implies that Best Place To Buy Kratom Leaf the live cells have taken up more PI thus increasing the DNA staining intensity. At this stage the possible explanation for this phenomenon is unknown however; it could be due to the plasma membrane integrity being compromised due the treatment effects thus creating pores or increase membrane permeabilisation. Numerous studies have shown that wild-type p53 can restrain cell cycle progression and induce cell death via apoptosis when the cell is irreversibly damage (Sugrue et al 1997). WAF 1 is a p53 target gene and both are well known to have positive correlation with cell cycle arrest (Morgan 2007; Harper et al 1993).
Cell Death Diff. Participation of p53 protein in the cellular response to DNA damage. Cancer Research 51:6304-6311. New apoptosis cascase mediated by lysosomal enzyme and its protection by epigallocatechin gallate. I and Mishra R. Biochemical and Biophysical Research Communications 137 813-820. Apoptosis: a basic biological phenomenon with wide ranging implications in tissue kinetics.
P21 is one of the main target genes for p53
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and both p53 and p21 are well known to have a positive correlation in assisting the cycle arrest by inhibiting the cyclinCdks complex formation (Morgan 2007). Based on these observations two possibilities are considered: 1) the effect is cell cycle arrest independent of p53 and p21 pathway or 2) the loss of these proteins could be due to the leakage due to the increased membrane permeability or through pore opening. The toxicity findings noted thus far are consistent with my hypothesis in which the dose is the main factor in determining the level of the cytotoxicity seen. The cytotoxicity events initially seen as cell cycle arrest proceed to cell death with increasing doses of MSE and MIT. My investigations of morphological microscopic examination on three different cell lines showed different modes of cell death. Prominent apoptotic-like cell death is mainly observed for SH-SY5Y cells and a necrotic type of cell death for the MCL-5 and HEK-293 cells. Further confirmation on these findings in differentiating the stages of cell death was carried out using Annexin V conjugate assay via flow cytometry analysis with SH-SY5Y and MCL-5 cells.