ABSTRACT
Apoptosis involves a phenomenon termed mitochondrial permeability transition (MPT) which induces permeability of a voltage-dependent pore to solutes of smaller than 1500Da. Induction of MPT pore is beneficial in case of tumour cells while inhibition of the pore is relevant in conditions such as tissue wastage. The effects of methanol extracts of Buccholzia coriacea (MEBC) commonly known as 'wonder kola' on MPT wa s assessed in vitro in normal rats inthe presence and absence of exogenous calcium- the triggering agent. MPT was estimated by the extent of mitochondrial swelling monitored spectrophotometrically as decreases in absorbance at 540nm. The results revealed that in the absence ofexogenous calcium, MPT pore opening was induced by MEBC at 200 microg/ml, 600 microg/ml, 1000 microg/ml and 1400 microg/ml in a concentration-dependent manner by 21.0, 7.6, 4.2, 3.5 folds, although higher concentrations of MEBC reduced pore opening. Pre-incubation of mitochondria with similar concentrations of MEBC for 5 minutes in the absence of calcium induced pore opening by 1.47, 10, 8.7 and 10.1 folds, respectively. Furthermore, mitochondrial membrane treated with MEBC (200 microg/ml, 600 microg/ml, 1000 microg/ml and 1400 microg/ml) in the presence of exogenous calcium induced pore opening by 63.9%, 44.0%, 23.4% and 64.4%, respectively. Oral administration of MEBC at varying doses of 50 - 200mg/kg b.w to rats for 30 days had no significant effects (p>0.05) on MPT pore opening in the absence of calcium when compared to untreated animals. The liver function tests revealed that the activities of alanine and aspartate amino transferases, alkaline phosphatase, and ã-glutammyl transferase were significantly (p>0.05) increased in serum of animals exposed to MEBC compared to control animals. Overall, Buccholzia coriacea induced MPT pore opening in vitro thus suggesting that certain bioactive components in the extract may prove useful in chemotherapy of tumor cells however, these bioactive agents seem to have been completely metabolized in vivo.
