Protein Information

Name caspase 3
Synonyms Apopain; CASP 3; CASP3; CPP 32; CPP32; CPP32B; Caspase 3; Caspase 3 precursor…

Compound Information

Name paraquat
CAS 1,1′-dimethyl-4,4′-bipyridinium

Reference List

PubMed Abstract RScore(About this table)
17509817 Kang X, Chen J, Xu Z, Li H, Wang B: Protective effects of Ginkgo biloba extract on paraquat-induced apoptosis of PC12 cells. Toxicol In Vitro. 2007 Sep;21(6):1003-9. Epub 2007 Feb 21.

Moreover, EGb761 pretreatment evidently increased the numbers of tyrosine hydroxylase (TH) positive and bcl-2 positive cells and degraded the number of caspase-3 positive cells in PQ-injured PC12 cells, in comparison to the treatment with PQ alone.
2(0,0,0,2) Details
18836921 Moran JM, Gonzalez-Polo RA, Ortiz-Ortiz MA, Niso-Santano M, Soler G, Fuentes JM: Identification of genes associated with paraquat-induced toxicity in SH-SY5Y cells by PCR array focused on apoptotic pathways. J Toxicol Environ Health A. 2008;71(22):1457-67.

Our analysis of apoptotic process through microarray technology showed that in PQ-induced neuroblastoma SH-SY5Y cells, there is a different expression of BIK, CASP3, CASP7, CRADD, DAPK, FAS, and other related genes, in comparison to unstimulated cells.
1(0,0,0,1) Details
17220179 Ungvari Z, Orosz Z, Rivera A, Labinskyy N, Xiangmin Z, Olson S, Podlutsky A, Csiszar A: Resveratrol increases vascular oxidative stress resistance. Am J Physiol Heart Circ Physiol. 2007 May;292(5):H2417-24. Epub 2007 Jan 12.

We found that oxidized LDL and TNF-alpha elicited significant increases in caspase-3/7 activity in endothelial cells and cultured rat aortas, which were prevented by resveratrol pretreatment (10 (-6)-10 (-4) mol/l).
Indeed, resveratrol treatment protected cultured aortic segments and/or endothelial cells against increases in intracellular H (2) O (2) levels and H (2) O (2)-mediated apoptotic cell death induced by oxidative stressors (exogenous H (2) O (2), paraquat, and UV light).
1(0,0,0,1) Details
18235974 Chen P, Li A, Zhang M, He M, Chen Z, Wu X, Zhao C, Wang S, Liang L: Protective effects of a new metalloporphyrin on paraquat-induced oxidative stress and apoptosis in N27 cells. Acta Biochim Biophys Sin. 2008 Feb;40(2):125-32.

In addition, our data provide direct evidence that MnTDM suppressed PQ-induced caspase-3 cleavage, possibly a key event of PQ neurotoxicity.
1(0,0,0,1) Details
17561093 Dinis-Oliveira RJ, Sousa C, Remiao F, Duarte JA, Ferreira R, Sanchez Navarro A, Bastos ML, Carvalho F: Sodium salicylate prevents paraquat-induced apoptosis in the rat lung. . Free Radic Biol Med. 2007 Jul 1;43(1):48-61. Epub 2007 Mar 24.

PQ-exposed rats suffered a time-dependent increase of caspase-3 and caspase-8 and a decrease of caspase-1 activities in lungs compared to the control group.
1(0,0,0,1) Details
17936647 Hou RR, Chen JZ, Chen H, Kang XG, Li MG, Wang BR: Neuroprotective effects of (-)-epigallocatechin-3-gallate (EGCG) on paraquat-induced apoptosis in PC12 cells. Cell Biol Int. 2008 Jan;32(1):22-30. Epub 2007 Sep 1.

The possible mechanism may be associated with maintaining mitochondrial membrane potential, inhibiting caspase-3 activity and downregulating the expression of pro-apoptotic protein Smac in cytosol.
1(0,0,0,1) Details
18056701 Fei Q, McCormack AL, Di Monte DA, Ethell DW: Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. . J Biol Chem. 2008 Feb 8;283(6):3357-64. Epub 2007 Dec 4.

PQ induced morphological and biochemical features that were consistent with apoptosis, including dose-dependent cytochrome c release, with subsequent caspase-3 and poly (ADP-ribose) polymerase cleavage.
1(0,0,0,1) Details
11413228 Ciriolo MR, Aquilano K, De Martino A, Carri MT, Rotilio G: Differential role of superoxide and glutathione in S-nitrosoglutathione-mediated apoptosis: a rationale for mild forms of familial amyotrophic lateral sclerosis associated with less active Cu,Zn superoxide dismutase mutants. J Neurochem. 2001 Jun;77(6):1433-43.

Cytochrome c release from mitochondria, caspase 3 activation, p53 up-regulation, p21 cleavage and Bcl-2 modulation, all involved in the apoptotic process, were significantly less altered with respect to untransfected cells.
On the other hand, H46R cells were as sensitive as SH-SY5Y cells to puromycin-induced apoptosis; furthermore, they were more susceptible to apoptosis elicited by the superoxide-generating drug paraquat and to cell necrosis provoked by t-butyl hydroperoxide.
1(0,0,0,1) Details
19735704 Yang W, Tiffany-Castiglioni E, Koh HC, Son IH: Paraquat activates the IRE1/ASK1/JNK cascade associated with apoptosis in human neuroblastoma SH-SY5Y cells. Toxicol Lett. 2009 Dec 15;191(2-3):203-10. Epub 2009 Sep 6.

0(0,0,0,0) Details
17018646 Ramachandiran S, Hansen JM, Jones DP, Richardson JR, Miller GW: Divergent mechanisms of paraquat, MPP+, and rotenone toxicity: oxidation of thioredoxin and caspase-3 activation. Toxicol Sci. 2007 Jan;95(1):163-71. Epub 2006 Oct 3.
112(1,2,2,2) Details
11369509 Rossi L, Marchese E, Lombardo MF, Rotilio G, Ciriolo MR: Increased susceptibility of copper-deficient neuroblastoma cells to oxidative stress-mediated apoptosis. Free Radic Biol Med. 2001 May 15;30(10):1177-87.

The mechanism underlying paraquat-triggered apoptosis implies dramatic activation of caspase-3 and induction of the transcription factor p53.
82(1,1,1,2) Details
12654481 Cheng WH, Quimby FW, Lei XG: Impacts of glutathione peroxidase-1 knockout on the protection by injected selenium against the pro-oxidant-induced liver aponecrosis and signaling in selenium-deficient mice. Free Radic Biol Med. 2003 Apr 1;34(7):918-27.

The paraquat-mediated gene or protein expression of proapoptotic Bax, Bcl-w, and Bcl-X (S), cell survival/death factors GADD45, MDM2, c-Myc, and caspase-3 was upregulated, but that of antiapoptotic Bcl-2 was downregulated in the GPX1-/- mice vs. the WT mice.
81(1,1,1,1) Details
19101702 Chau KY, Korlipara LV, Cooper JM, Schapira AH: Protection against paraquat and A53T alpha-synuclein toxicity by cabergoline is partially mediated by dopamine receptors. J Neurol Sci. 2009 Mar 15;278(1-2):44-53. Epub 2008 Dec 21.

Cabergoline increased glutathione content, reduced free radical production and caspase-3 activation, increased mitochondrial membrane potential and ameliorated cell death in SHSY-5Y cells exposed to paraquat and this action was inhibited in part by D2 receptor blockade.
31(0,1,1,1) Details
18365879 Rio MJ, Velez-Pardo C: Paraquat induces apoptosis in human lymphocytes: protective and rescue effects of glucose, cannabinoids and insulin-like growth factor-1. Growth Factors. 2008 Feb;26(1):49-60.

Further evaluation included (i) superoxide radicals, reflected by nitroblue tetrazolium reduction to formazan, (ii) the production of hydrogen peroxide, reflected by rhodamine-positive fluorescent cells, (iii) the generation of hydroxyl radicals, reflected by dimethylsulfoxide and melatonin ( radical) OH scavengers, (iv) activation and/or translocation of NF-kappaB, p53 and c-Jun transcription factors showed by immunocytochemical staining, and by ammonium pyrrolidinedithiocarbamate, pifithrin-alpha and SP600125 inhibition and (V) caspase-3 activation, reflected by caspase Ac-DEVD-cho inhibition.
3(0,0,0,3) Details
11181820 Chun HS, Gibson GE, DeGiorgio LA, Zhang H, Kidd VJ, Son JH: Dopaminergic cell death induced by MPP (+), oxidant and specific neurotoxicants shares the common molecular mechanism. J Neurochem. 2001 Feb;76(4):1010-21.

Epidemiological risk factor analyses of typical PD cases have identified several neurotoxicants, including MPP (+) (the active metabolite of MPTP), paraquat, dieldrin, manganese and salsolinol.
Remarkably, the oxidant treatment alone induced similar sequential molecular events: ROS increase, activation of JNK MAP kinases, activation of the PITSLRE kinase, p110, by both Caspase-1 and Caspase-3-like activities and apoptotic cell death.
1(0,0,0,1) Details
15157803 Gonzalez-Polo RA, Rodriguez-Martin A, Moran JM, Niso M, Soler G, Fuentes JM: Paraquat-induced apoptotic cell death in cerebellar granule cells. Brain Res. 2004 Jun 18;1011(2):170-6.

Exposure of cerebellar granule cells to relatively low concentrations of paraquat (5 microM) produces apoptotic cell death with a reduction in mitochondrial cytochrome c content, proteolytic activation and caspase-3 activity increase and DNA fragmentation.
31(0,1,1,1) Details
15155744 Peng J, Mao XO, Stevenson FF, Hsu M, Andersen JK: The herbicide paraquat induces dopaminergic nigral apoptosis through sustained activation of the JNK pathway. J Biol Chem. 2004 Jul 30;279(31):32626-32. Epub 2004 May 20.

Our data show that paraquat induces the sequential phosphorylation of c-Jun N-terminal kinase (JNK) and c-Jun and the activation of caspase-3 and sequential neuronal death both in vitro and in vivo.
31(0,1,1,1) Details