Protein Information

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

Compound Information

Name sodium arsenite
CAS sodium arsenenite

Reference List

PubMed Abstract RScore(About this table)
17681577 Lin AM, Chao PL, Fang SF, Chi CW, Yang CH: Endoplasmic reticulum stress is involved in arsenite-induced oxidative injury in rat brain. Toxicol Appl Pharmacol. 2007 Oct 15;224(2):138-46. Epub 2007 Jul 3.

For mitochondrial activation, cytosolic cytochrome c and caspase-3 levels were elevated in the arsenite-infused SN.
The mechanism underlying sodium arsenite (arsenite)-induced neurotoxicity was investigated in rat brain.
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12472888 Fauconneau B, Petegnief V, Sanfeliu C, Piriou A, Planas AM: Induction of heat shock proteins (HSPs) by sodium arsenite in cultured astrocytes and reduction of hydrogen peroxide-induced cell death. J Neurochem. 2002 Dec;83(6):1338-48.

TdT-mediated dUTP nick-end labelling (TUNEL) reaction and caspase-3 activation.
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19429265 Das J, Ghosh J, Manna P, Sinha M, Sil PC: Taurine protects rat testes against NaAsO (2)-induced oxidative stress and apoptosis via mitochondrial dependent and independent pathways. Toxicol Lett. 2009 Jun 22;187(3):201-10. Epub 2009 Mar 14.


In this study, we report that As administration (in the form of NaAsO (2) at a dose of 10mg/kg body weight for 2 days, orally) induces apoptosis in testicular tissue of the experimental rats by the activation of caspase-3 and reciprocal regulation of Bcl-2/Bad with the concomitant reduction of mitochondrial membrane potential and increased level of cytosolic cytochrome C.
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13129816 Yeh JY, Cheng LC, Liang YC, Ou BR: Modulation of the arsenic effects on cytotoxicity, viability, and cell cycle in porcine endothelial cells by selenium. Endothelium. 2003;10(3):127-39.

MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay indicated that arsenic trioxide (As (2) O (3)) and sodium arsenite (NaAsO (2)) showed similar cytotoxicity, whereas sodium arsenate (Na (2) HAsO (4)) did not show cytotoxicity in PAECs.
As (2) O (3)-induced apoptosis was associated with upregulation of p53 and caspase 3, whereas NaAsO (2)-induced apoptosis was associated with p53 upregulation.
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18715270 Lin AM, Feng SF, Chao PL, Yang CH: Melatonin inhibits arsenite-induced peripheral neurotoxicity. J Pineal Res. 2009 Jan;46(1):64-70. Epub 2008 Aug 18.

At the same time, melatonin inhibited arsenite-induced activation of caspase 3 in the treated DRG explants.
In this study, the effect of melatonin on sodium arsenite (arsenite)-induced peripheral neurotoxicity was investigated using dorsal root ganglion (DRG) explants.
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16079067 Wu F, Burns FJ, Zhang R, Uddin AN, Rossman TG: Arsenite-induced alterations of DNA photodamage repair and apoptosis after solar-simulation UVR in mouse keratinocytes in vitro. Environ Health Perspect. 2005 Aug;113(8):983-6.

The keratinocytes were treated with different concentrations of sodium arsenite (0.0, 2.5, 5.0 microM) for 24 hr and then were immediately irradiated with a single dose of 0.30 kJ/m2 UVR.
Arsenite decreased the UVR-induced caspase-3/7 activity in parallel with the inhibition of apoptosis.
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18501396 McNeely SC, Taylor BF, States JC: Mitotic arrest-associated apoptosis induced by sodium arsenite in A375 melanoma cells is BUBR1-dependent. Toxicol Appl Pharmacol. 2008 Aug 15;231(1):61-7. Epub 2008 Apr 9.

Mitotic arrest resulted in apoptosis as indicated by colocalization of mitotic phospho-Histone H3 with active caspase 3.
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12676792 Mathas S, Lietz A, Janz M, Hinz M, Jundt F, Scheidereit C, Bommert K, Dorken B: Inhibition of NF-kappaB essentially contributes to arsenic-induced apoptosis. Blood. 2003 Aug 1;102(3):1028-34. Epub 2003 Apr 3.


In these cell lines, apoptosis was blocked by inhibition of caspase-8 and caspase-3-like activity.
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15737492 Ramanathan K, Anusuyadevi M, Shila S, Panneerselvam C: Ascorbic acid and alpha-tocopherol as potent modulators of apoptosis on arsenic induced toxicity in rats. Toxicol Lett. 2005 Apr 10;156(2):297-306. Epub 2005 Jan 13.


The present work was conducted to evaluate the regulatory effect exerted by Vitamin C and Vitamin E upon the apoptotic process, which can be assessed by the presence of cells with apoptosis associated DNA breaks and characterize the role of TNF-alpha and caspase-3 in rats intoxicated with arsenic.
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11813266 Chou RH, Huang H: Sodium arsenite suppresses human papillomavirus-16 E6 gene and enhances apoptosis in E6-transfected human lymphoblastoid cells. J Cell Biochem. 2002;84(3):615-24.

After arsenite treatment, TK6-E6 cells showed more sub-G1 apoptosis, activated caspase-3/CPP32 fragment, DNA ladder, and less viability than parental TK6 cells, indicating that arsenite enhanced apoptosis in E6-transfected TK6 cells.
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16251481 Sidhu JS, Ponce RA, Vredevoogd MA, Yu X, Gribble E, Hong SW, Schneider E, Faustman EM: Cell cycle inhibition by sodium arsenite in primary embryonic rat midbrain neuroepithelial cells. Toxicol Sci. 2006 Feb;89(2):475-84. Epub 2005 Oct 26.

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10652248 Mirkes PE, Little SA: Cytochrome c release from mitochondria of early postimplantation murine embryos exposed to 4-hydroperoxycyclophosphamide, heat shock, and staurosporine. Toxicol Appl Pharmacol. 2000 Feb 1;162(3):197-206.

Previously, we showed that the cell death induced in day 9 mouse embryos by three teratogens, hyperthermia (HS), 4-hydroperoxycyclophosphamide (4-CP), and sodium arsenite (As), is apoptotic in nature involving the activation of caspase-3, cleavage of poly (ADP-ribose) polymerase (PARP), and DNA fragmentation.
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15130612 Greenlee AR, Kronenwetter-Koepel TA, Kaiser SJ, Ellis TM, Liu K: Combined effects of Matrigel and growth factors on maintaining undifferentiated murine embryonic stem cells for embryotoxicity testing. Toxicol In Vitro. 2004 Aug;18(4):543-53.

Early-passage cells showed dose-responsive caspase-3 activation following exposure to sodium arsenite, whereas caspase-3 activation of late-passage cells dropped to background levels at toxicant dosages above 50 ppb.
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10200514 Mirkes PE, Little SA: Teratogen-induced cell death in postimplantation mouse embryos: differential tissue sensitivity and hallmarks of apoptosis. Cell Death Differ. 1998 Jul;5(7):592-600.

We show that three teratogens, hyperthermia, cyclophosphamide and sodium arsenite induce an increase in cell death in day 9.0 mouse embryos with concurrent induction of DNA fragmentation, activation of caspase-3 and the cleavage of poly (ADP-ribose) polymerase (PARP).
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16497974 Che XF, Zheng CL, Owatari S, Mutoh M, Gotanda T, Jeung HC, Furukawa T, Ikeda R, Yamamoto M, Haraguchi M, Arima N, Akiyama S: Overexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines. Blood. 2006 Jun 15;107(12):4880-7. Epub 2006 Feb 23.

Sodium arsenite was shown to down-regulate the expression of survivin at both the protein and RNA levels in a time- and dose-dependent manner, thus inhibiting cell growth, inducing apoptosis, and enhancing the caspase-3 activity in ATL cells.
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15713546 Greenlee AR, Kronenwetter-Koepel TA, Kaiser SJ, Liu K: Comparison of Matrigel and gelatin substrata for feeder-free culture of undifferentiated mouse embryonic stem cells for toxicity testing. Toxicol In Vitro. 2005 Apr;19(3):389-97. Epub 2005 Jan 21.

In other comparisons, however, Matrigel supported significantly higher synthesis of alkaline phosphatase (7.7x10 (-3)+/-0.8 vs 6.6x10 (-3)+/-0.8 units/liter/cell, respectively, P=0.012), overall expression of activated caspase-3 following exposure to 5, 10, 50, 100 and 500 parts per billion (ppb) sodium arsenite (P <0.0001), and percent development to beating cardiomyocytes at P7 (P=0.01).
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17849503 Watcharasit P, Thiantanawat A, Satayavivad J: GSK3 promotes arsenite-induced apoptosis via facilitation of mitochondria disruption. J Appl Toxicol. 2008 May;28(4):466-74.


Investigation of the involvement of GSK3 in arsenite-induced apoptosis demonstrated that arsenite induced apoptosis in SH-SY5Y human neuroblastoma cells, activating the executioner caspase-3 which caused cleavage of poly-ADP ribose-polymerase (PARP).
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16433889 Bashir S, Sharma Y, Irshad M, Gupta SD, Dogra TD: Arsenic-induced cell death in liver and brain of experimental rats. Basic Clin Pharmacol Toxicol. 2006 Jan;98(1):38-43.

Sodium arsenite was administered orally at doses of 6.3 mg/kg, 10.5 mg/kg and 12.6 mg/kg of body weight on the basis of a lethal dose 50% (LD50) for 24 hr.
After administration of arsenites, liver and brain were analyzed for various parameters of oxidative stress, histopathological changes and caspase-3 activity.
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19616567 Ghosh J, Das J, Manna P, Sil PC: Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: role of NF-kappa B, p38 and JNK MAPK pathway. Toxicol Appl Pharmacol. 2009 Oct 1;240(1):73-87. Epub 2009 Jul 17.


Arsenic reduced cardiomyocyte viability, increased reactive oxygen species (ROS) production and intracellular calcium overload, and induced apoptotic cell death by mitochondrial dependent caspase-3 activation and poly-ADP ribose polymerase (PARP) cleavage.
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12503296 Zeng L, Smith LD: Caspase-3 colorimetric assay. Biotechniques. 2002 Dec;33(6):1196-7.

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15377153 Lee CH, Yu CL, Liao WT, Kao YH, Chai CY, Chen GS, Yu HS: Effects and interactions of low doses of arsenic and UVB on keratinocyte apoptosis. Chem Res Toxicol. 2004 Sep;17(9):1199-205.

The caspase-3, -8, and -9 relative activities were all increased in the UVB group; however, arsenic significantly enhanced caspase-8 and -3 relative activities in UVB-irradiated keratinocytes (the UVB-As group).
Cultured human keratinocytes were treated with sodium arsenite (1 microM) and/or UVB (50 mJ/cm (2)) irradiation in different combinations: (i) arsenic alone, (ii) UVB alone, (iii) arsenic followed by UVB (As-UVB), and (iv) UVB followed by arsenic (UVB-As) treatments.
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19082730 Chowdhury R, Chowdhury S, Roychoudhury P, Mandal C, Chaudhuri K: Arsenic induced apoptosis in malignant melanoma cells is enhanced by menadione through ROS generation, p38 signaling and p53 activation. Apoptosis. 2009 Jan;14(1):108-23.


MATERIALS METHODS AND RESULTS: Menadione synergized NaAsO (2) to significantly increase ROS generation and facilitate the major apoptotic signaling events: alteration of mitochondrial membrane potential, cytochrome c release and anti-apoptotic protein Bcl-2 down-regulation and subsequent activation of caspase-9 and caspase-3 followed by poly-ADP-ribose polymerase-1 cleavage.
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19536524 Wang Y, Xu Y, Wang H, Xue P, Li X, Li B, Zheng Q, Sun G: Arsenic induces mitochondria-dependent apoptosis by reactive oxygen species generation rather than glutathione depletion in Chang human hepatocytes. Arch Toxicol. 2009 Oct;83(10):899-908. Epub 2009 Jun 18.

The MTT assay demonstrated that sodium arsenite (NaAsO2) treatment for 24 h caused a dose-dependent decrease of cell viability.
NaAsO2 treatment (0-30 microM) was also found to induce phosphatidylserine externalization, a hallmark of apoptosis; to disrupt the mitochondrial membrane potential (Deltapsi ( m )); to cause the release of cytochrome c into the cytosol, and to trigger cleavage of caspase-3 and poly (ADP-ribose) polymerase (PARP) in a dose-dependent manner.
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17645694 Lin AM, Fang SF, Chao PL, Yang CH: Melatonin attenuates arsenite-induced apoptosis in rat brain: involvement of mitochondrial and endoplasmic reticulum pathways and aggregation of alpha-synuclein. J Pineal Res. 2007 Sep;43(2):163-71.

In the present study, the protective effect of melatonin on sodium arsenite (arsenite)-induced apoptosis was investigated.
In the mitochondrial pathway, systemic melatonin inhibited arsenite-induced elevations in Bcl-2 and cytosolic cytochrome c as well as arsenite-induced reductions in procaspase-3 levels and elevations in active caspase-3 levels in the infused SN.
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