P53, Bax and Cathepsin D Dysregulation in Neurons Subjected to Cyanide Toxicity and Oxygen Deprivation

OGUNDELE, Olalekan Michael and ADEKEYE, Adeshina Oloruntoba and ADENIYI, Philip Adeyemi and OGEDENGBE, Oluwatosin Olalekan and ENYE, Linus Anderson and SAHEED, Sabiu and ANOSIKE, Victor Ikenna (2013) P53, Bax and Cathepsin D Dysregulation in Neurons Subjected to Cyanide Toxicity and Oxygen Deprivation. World J Life Sci. and Medical Research, 3 (1). pp. 1-6. ISSN 2249-0574

	Text en_wjlsmr_vol_3_iss_1_pg_33_38.pdf - Published Version Download (256kB)
	Text en_wjlsmr_vol_3_iss_1_pg_33_38.pdf Download (256kB)

Abstract

Cyanide is a potent neurotoxin capable of potentiation NMDA R1 (N-methyl-D-aspartate receptor 1) a form of glutamate receptor that is calcium gated, thus causing excitotoxicity. It is also well established that the glutamate-glucose exchange is dependent on the activity of the Na + /K + ATPase pump, thus we examine the role of the Na + /K + pump in the metabolism of the neuron during cyanide toxicity. Six separate perfusion set up of the rat brain cortical tissues were made with ACSF (ACSF, ACSF+KCN, ACSF+KCN + pump blocker, ACSF + pump blocker). The tissues were perfused for duration of 180 minutes. The tissues were processed immunohistochemically using antibodies against p53,Bax and Cathepsin D (CD) to demonstrate disregulation of cell cycle proteins associated with the induced DNAbreakage as a result of cyanide toxicity. The pumpblockers (methyldigoxin and promethazine) induced excitotoxicity when used in culture, and amplified cyanide toxicity when combined with KCN. Cell death induced by toxicity of cyanide and the blockade of the Na/K ATPasepump has been seen to be complimentary in driving the toxicity effects that drives the cell into apoptosis.The tumor suppressor/apoptosis inducing factors p53 and Bax were over expressed while cathepsin was suppressed to show that the cells are apoptotic as against an increased cathepsin D level that would have implied senescence.

Actions (login required)

View Item