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Is Kratom A Cns Depressant

Nature 366: 707-710. Cathepsin B kratom for withdrawal contributes to TNF-amediated hepatocytes apoptosis by promoting mitochondrial release of cytochrome c. Is Kratom A Cns Depressant the morphology of apoptosis.

The nature of cell death observed was unknown and to the best of my knowledge there are no reports or information available on Mitragyna speciosa Korth toxicity on mammalian cells. In this study therefore an attempt was made to characterise the MSE and MIT toxicity by looking at cell cycle distribution. Firstly attempt was made to look at the cell cycle distribution in different cell lines using flow cytometry approach. Propidium Iodide is one of the most common and recommended dyes to use to quantitatively assess DNA content by flow cytometry (Darzynkiewicz et al 2001). The dose response and temporal effects of treatment were examined in this assay in order to maximally evaluate the effect on the cell cycle. Cell cycle analysis was initially performed Is Kratom A Cns Depressant using HEK 293 cells and the DNA profile was determined manually using the Cellquest Pro software (Fig.

In determining the mechanism of cell death induced by MSE and MIT it was noted that MSE caused a different mode of cell death depending on cell type. Morphologically after MSE insult SH-SY5Y cells appeared to die via apoptosislike cell death whereas MCL-5 and HEK 293 cells show predominantly a necrotic type of cell death. Biochemical investigations confirmed that MSE induced SH-SY5Y cell death independent of p53 or caspases therefore the Is Kratom A Cns Depressant mechanism of apoptotic-like Is Kratom A Cns Depressant morphology features is not entirely clear however a few possible mechanisms for this type of cell death can be proposed. MIT induced cell death in SH-SY5Y cells appeared to be associated with p53 kratom illinois and caspasesdependant pathway however lacking morphological examinations restricts the confirmation of this finding. The study also confirmed that there was no involvement of ROS production in MSE and MIT induced cell death implying that mitochondrial integrity is not compromised.

TK- mouse lymphoma cells. Plymouth UK 2002. Genetic Toxicology and Environmental Mutagenesis 540:127-140. Cyclin-dependent kinases: engines clocks and microprocessors. Annu Rev Cell Dev Biol.

The American Journal of Addiction 16: 352-356. E McCurdy C. kratom 4 grams Self-treatment of opioid widrawal using kratom (Mitragyna speciosa Korth).

The intensity of the fluorescence is therefore proportional to the levels of intracellular ROS (Galvano et al 2002) –

  1. To further clarify the above finding S9 from rat liver (induced by Arochlor 1254) was used with SH-SY5Y and HEK-293 cells as these cells have no metabolic activity
  2. Measurement of ROS with DCFH-DA in SH-SY5Y cells treated with A) H202 MSE with or without NAC and and B) H202 MIT with or without NAC
  3. Wildtype p53 is a cell cycle checkpoint determinant following irradiation
  4. BMJ 332: 175-176 Weinert T
  5. Triplicate wells of 10% FBS media for control group were also added for comparison
  6. Single cultures were established for each treatment concentration and in triplicate for vehicle control

. A fluorescence-based method to measure ROS generation in live cells was a modification of the procedure described by Esposti and McLennan (1998). This is to ensure that the free-radical quencher albumin Is Kratom A Cns Depressant present in the serum used as a media supplement is removed as it interferes with the quantitative analysis of ROS (Esposti 2002).

Effects of MSE on the cell cycle distribution of SH-SY5Ycells after 48 hr of treatment. MSE on the cell cycle distribution of SH-SY5Y cells at different time points (4 8 24 48 72 and 96 hr treatment). Indicates only one experimental result.

There are no reports of increased cancer associated with consumption of Kratom leaves although such associations have never been examined in a proper controlled study. Neither is there any information available concerning the genotoxic potential of Kratom leaves. As part of establishing a database on the toxicological potential of the use of this plant I have attempted to examine the possible toxicological effects this plant might have including potential for carcinogenicity via genotoxicity testing. The basic toxicology data established in the previous chapter has informed us on the potential cytotoxicity of MSE and MIT on several human cell lines which generally shows cytotoxicity with high dose. The lethal effect of the extract and major alkaloid (MIT) on the cells examined

Is Kratom A Cns Depressant

prompted the question whether cell death was accompanied by DNA damage. DNA damage as a result of endogenous sources (cellular metabolic processes) or exogenous sources (environmental factors such as chemical insult) could lead to reversible or irreversible genetic change. Based on the Is Kratom A Cns Depressant long term use of this plant by humans testing for its genotoxic potential using mammalian cells was thought to be more appropriate than conventional first tier testing for gene mutation primo indo kratom effects in bacteria.

Food and Chemical Toxicology 40: 25-31. Lost in transcription: p21 repression mechanisms and consequences. Cancer Research 65:3980-3985. Targeting apoptosis pathways in cancer therapy. CA Cancer J Clin.

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