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Therefore the possible involvement of the caspase enzymes
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such as upstream caspases 8 and 9 which are involved in both intrinsic and extrinsic pathways and also the executioner caspases 3 and 7 were investigated. MSE mediated cell death was found to not involve any of the caspase
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cascades examined. Thus this finding is consistent indo kratom export ban with the previous data which indicates that the apoptotic-like cell death seen for MSE treated SH-SY5Y

cells is p53independent and caspase independent. Buy Kratom In Bolton Landing Ny 12814 other pathways may be considered for MSE induced cell death with no involvement of caspase activation but yet following the programmed fashion.

A kratom golden extract capsule second incubation time point at 18 hr also showed negative results. The next step was investigating the possibility of involvement of executioner caspases such as caspase 3 and 7. The executioner caspases are also known as downstream caspases as they depend on active initiator caspases for their activation by proteolytic cleavage Buy Kratom In Bolton Landing Ny 12814 (Srinivasula et al 2001):

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  • Interestingly whilst S9 did not potentiate MIT toxicity prolonged exposure of the cells to MIT did appear to induce dose-dependant toxicity

. As anticipated there was no activation of caspases 3 and 7 activities in cells treated with high dose of MSE at both 4 hr and 18 hr incubation time points. Interestingly for MIT there was a clear kratom drug test kit significant difference of caspases 3 and 7 activities at both concentrations of MIT tested. This finding suggests that the mode of the cell death of MIT treated cells is dependant on caspase 3 and 7 activation pathway. There were no significant differences in the subG1 population (apoptosis population) between treated groups (caspase 3 inhibitor caspase 8 inhibitor caspase 9 inhibitor and general caspase inhibitor treated with high dose of MSE) and the control and negative control groups.

As shown in fig. A there was a non-significant difference noted for caspase 3 and 7 activities for MSE treated cells compared to control groups at 4 hr incubation time point. For MIT treated cells (Fig.

The level of MSE toxicity for SH-SY5Y and HEK 293 cells was found to be increased 10-fold when metabolic activation system (post mitochondrial rat liver S9 induced

with Arochlor 1254) was added to the treatment. This implies that MSE cytotoxicity requires metabolism for its activation and CYP2E1 was thought to be involved in this metabolic activation. However MIT in parallel experiments did not show any enhancement of toxicity in the presence of S9 and was inherently cytotoxic.

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