| Name | caspase (protein family or complex) |
|---|---|
| Synonyms | caspase; caspases |
| Name | parathion |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12518333 | Saleh AM, Vijayasarathy C, Fernandez-Cabezudo M, Taleb M, Petroianu G: Influence of paraoxon (POX) and parathion (PAT) on apoptosis: a possible mechanism for toxicity in low-dose exposure. J Appl Toxicol. 2003 Jan-Feb;23(1):23-9. We examined cellular responses, including induction of apoptosis, involvement of a caspase cascade, the activity of effector caspase (caspase-3) and the biochemical and morphological changes that are the hallmarks of classical apoptosis. |
1(0,0,0,1) | Details |
| 19911945 | Fukuyama T, Tajima Y, Ueda H, Hayashi K, Shutoh Y, Harada T, Kosaka T: Apoptosis in immunocytes induced by several types of pesticides. J Immunotoxicol. 2010 Mar;7(1):39-56. Thymocytes and J45.01 cells were treated for 4 or 8 hr with varying doses of metamidophos, parathion, PNMC, or methoxychlor; dexamethasone was used as a positive control. Apoptosis, cell viability, the proportion of Annexin-V+ cells, the activities of caspases 3/7, 8, and 9, and the levels of DNA fragmentation in both the J45.01 cells and thymocytes were then examined. |
1(0,0,0,1) | Details |
| 11032765 | Carlson K, Jortner BS, Ehrich M: Organophosphorus compound-induced apoptosis in SH-SY5Y human neuroblastoma cells. Toxicol Appl Pharmacol. 2000 Oct 15;168(2):102-13. Pretreatment with the serine protease inhibitor phenylmethyl sulfonyl (PMSF; 1 mM, 8 h) also significantly decreased caspase activation following 1 mM PSP and TOTP exposures (p < 0.05). Hoechst staining revealed significant paraoxon (1 mM), parathion (1 mM), phenyl saligenin (PSP, 10 and 100 microM), tri-ortho-tolyl (TOTP, 100 microM and 1 mM), and triphenyl (TPPi, 1 mM) induced time-dependent increases in traditional apoptosis (p < 0.05). |
2(0,0,0,2) | Details |
| 12831782 | Saleh AM, Vijayasarathy C, Masoud L, Kumar L, Shahin A, Kambal A: Paraoxon induces apoptosis in EL4 cells via activation of mitochondrial pathways. Toxicol Appl Pharmacol. 2003 Jul 1;190(1):47-57. Recently, we have shown that, at noncholinergic doses (1 to 10 nM), POX (the bioactive metabolite of parathion) causes apoptotic cell death in murine EL4 T-lymphocytic leukemia cell line through activation of caspase-3. In this study, by employing caspase-specific inhibitors, we extend our observations to elucidate the sequence of events involved in POX-stimulated apoptosis. |
2(0,0,0,2) | Details |