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White Sumatran Kratom Central City

For 24 hr results there were no apparent changes in the DNA profile between the control and low dose of MSE (11. White Sumatran Kratom Central City mSE as the profile was completely destroyed. Increasing subG1 phase was noted for all dose ranges tested at 48 hr treatment period indicating an increase of the toxicity over time. The subG1 phase has been proposed to be a population of apoptotic cells (Darzynkiewicz et al 1992).

The trypan blue assay and clonogenicity assay were employed as described in chapter 2 section 2. MSE and MIT are discussed as follows: Effects of naloxone on MSE and MIT treated cells: Fig. Naloxone also appears to successfully inhibit the MIT toxicity (Fig. However on the longer term effects of treatment (clonogenicity assay) as shown in fig.

Nature 366: 707-710. Cathepsin B contributes to TNF-amediated hepatocytes apoptosis by promoting mitochondrial release of cytochrome c. The morphology of apoptosis.

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 mitragyna speciosa – maeng da thai kratom agents. Thus the findings of this study will hopefully contribute to a better understanding in predicting the risk upon consuming Mitragyna speciosa Korth leaves. M human consumption 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

White Sumatran Kratom Central City

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 to be enhanced by metabolism particularly by CYP 2E1. Thus the combination consumption of Mitragyna speciosa Korth leaves with CYP 2E1 inducers may White Sumatran Kratom Central City 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.

M MIT where cells accumulated at G1 phase and the population shifted to the right side of the scale. This phenomenon implies that the treated cells have taken up more PI dye thus leading to a shift to the right. Due to the amount of MIT compound available repetition of this experiment was not possible. Effects of MSE on the cell cycle distribution of SH-SY5Ycells after 48 hr of treatment.

M concentration also gave some protection against MSE toxicity at high dose but not sufficient to be significant when kratom extract everclear compared to Control groups. D) it appears that naltrindole again successfully inhibited MIT toxicity at all concentrations tested. Whereas for the longer term effects (clonogenicity assay) fig. M successfully gave protection against MSE toxicity at all dose range however it was not that effective for MIT at high dose. MSE mediates its toxicity via this receptor as shown in acute treatment of MSE (trypan blue exclusion Fig. E) giving protection against MSE toxicity at high dose. F cyprodime hydrobromide also gave some protection effects against MIT toxicity (as measured by trypan blue exclusion).

Academic Press San Diego. ErlandssonHarris et al. High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokines sysnthesis in human monocytes. In vitro genotoxicity of kratom thai green vein the West African anti-malarial herbal cryptolepis sanguinolenta and its major alkaloid crytolepine. Molecular White Sumatran Kratom Central City dissection of mutations at the heterozygous thymidine kinase locus in mouse lymphoma cells. Targeting death and decoy receptors of the tumour-necrosis factor superfamily.

Introduction Cytotoxicity and genotoxicity status of MSE and MIT were established in the previous chapters and both agents were determined to be toxic at high dose but not genotoxic. The molecular events leading to toxicity are yet to be fully understood. Cell cycle is an essential process for all living organisms with the ultimate goal to create new cells necessary for maintaining continued survival. Under normal circumstances the four phases of the cell cycle G1 White Sumatran Kratom Central City S G2 and M phases are tightly regulated. The entry of the cell into each phase of cell cycle is carefully regulated by cell cycle checkpoints which act as the cell cycle control systems.

B MIT Treatment without S9 (24 hr) Neg. C 30 20 10 5 MMS Cell conc. Relative suspension growth (RSG) 100. Summary table of MLA result for MIT in the i) presence of rat liver S9 and ii) in the

White Sumatran Kratom Central City

absence of rat liver S9. S9 treatment Treatment groups Negative control 0 0 0 30 20 MIT 10 5 Positive control (DMBA) Mean Control MF 76. Negative Negative Negative Negative Negative Negative Negative Positive Conc.

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