Protein Information

Name heme oxygenase 1
Synonyms HMOX 1; HMOX1; HMOX1 protein; HO; HO 1; HO1; Heme oxygenase (Decycling) 1; Heme oxygenase (Decyclizing) 1…

Compound Information

Name carbon tetrachloride
CAS tetrachloromethane

Reference List

PubMed Abstract RScore(About this table)
17173083 Wen T, Zhao JY, Mei S, Guan L, Zhang YL: [Protective effect of heme oxygenase-1 and its reaction product, carbon monoxide on acute liver injury induced by carbon tetrachloride in rats]. Beijing Da Xue Xue Bao. 2006 Dec 18;38(6):618-22.
172(2,2,3,7) Details
16978757 Wen T, Guan L, Zhang YL, Zhao JY: Dynamic changes of heme oxygenase-1 and carbon monoxide production in acute liver injury induced by carbon tetrachloride in rats. Toxicology. 2006 Nov 10;228(1):51-7. Epub 2006 Aug 22.
86(1,1,1,6) Details
17275847 Eipel C, Eisold M, Schuett H, Vollmar B: Inhibition of heme oxygenase-1 protects against tissue injury in carbon tetrachloride exposed livers. J Surg Res. 2007 May 1;139(1):113-20. Epub 2007 Feb 1.
36(0,1,1,6) Details
16309569 Immenschuh S, Fahimi HD, Baumgart-Vogt E: Complementary regulation of heme oxygenase-1 and peroxiredoxin I gene expression by oxidative stress in the liver. Cell Mol Biol (Noisy-le-grand). 2005 Oct 3;51(5):471-7.

Moreover, expression of the HO-1 and Prx I genes was determined in a model of acutely damaged rat liver which was elicited by application of a single dose of carbon tetrachloride (CCl4).
13(0,0,1,8) Details
19060448 Mamiya T, Katsuoka F, Hirayama A, Nakajima O, Kobayashi A, Maher JM, Matsui H, Hyodo I, Yamamoto M, Hosoya T: Hepatocyte-specific deletion of heme oxygenase-1 disrupts redox homeostasis in basal and oxidative environments. Tohoku J Exp Med. 2008 Dec;216(4):331-9.

HO-1 CKO mice were susceptible to carbon tetrachloride hepatotoxicity.
13(0,0,1,8) Details
18547752 Yamaji K, Ochiai Y, Ohnishi K, Yawata A, Chikuma T, Hojo H: Up-regulation of hepatic heme oxygenase-1 expression by locally induced interleukin-6 in rats administered carbon tetrachloride intraperitoneally. Toxicol Lett. 2008 Jul 10;179(3):124-9. Epub 2008 May 2.
12(0,0,1,7) Details
16964402 Kawakami T, Takahashi T, Shimizu H, Nakahira K, Takeuchi M, Katayama H, Yokoyama M, Morita K, Akagi R, Sassa S: Highly liver-specific heme oxygenase-1 induction by interleukin-11 prevents carbon tetrachloride-induced hepatotoxicity. Int J Mol Med. 2006 Oct;18(4):537-46.
10(0,0,1,5) Details
17002867 Farombi EO, Surh YJ: Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol. 2006 Sep 30;39(5):479-91.

In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as acetaminophen, carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection.
10(0,0,1,5) Details
17879412 Xue H, Guo H, Li YC, Hao ZM: Heme oxygenase-1 induction by hemin protects liver cells from ischemia/reperfusion injury in cirrhotic rats. World J Gastroenterol. 2007 Oct 28;13(40):5384-90.

6(0,0,0,6) Details
17917259 Lee CH, Park SW, Kim YS, Kang SS, Kim JA, Lee SH, Lee SM: Protective mechanism of glycyrrhizin on acute liver injury induced by carbon tetrachloride in mice. Biol Pharm Bull. 2007 Oct;30(10):1898-904.

The levels of hepatic inducible nitric oxide synthase, cyclooxygenase-2, and heme oxygenase-1 protein expression were markedly higher after the CCl (4) treatment.
5(0,0,0,5) Details
16610050 Tsui TY, Lau CK, Ma J, Glockzin G, Obed A, Schlitt HJ, Fan ST: Adeno-associated virus-mediated heme oxygenase-1 gene transfer suppresses the progression of micronodular cirrhosis in rats. World J Gastroenterol. 2006 Apr 7;12(13):2016-23.

5(0,0,0,5) Details
16025519 Tsui TY, Lau CK, Ma J, Wu X, Wang YQ, Farkas S, Xu R, Schlitt HJ, Fan ST: rAAV-mediated stable expression of heme oxygenase-1 in stellate cells: a new approach to attenuate liver fibrosis in rats. Hepatology. 2005 Aug;42(2):335-42.

Portal injection of rAAVs to normal or carbon tetrachloride (CCl (4))-induced liver fibrosis showed a distinct distribution of rAAV binding.
4(0,0,0,4) Details
19793341 Quan J, Piao L, Wang X, Li T, Yin X: Rossicaside B protects against carbon tetrachloride-induced hepatotoxicity in mice. Basic Clin Pharmacol Toxicol. 2009 Dec;105(6):380-6. Epub 2009 Sep 30.

Furthermore, the contents of hepatic nitrite, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and haem oxygenase-1 (HO-1) were elevated after CCl (4) treatment while the cytochrome P450 2E1 (CYP2E1)-specific monooxygenase activity was suppressed.
3(0,0,0,3) Details
18187930 Park SW, Lee CH, Kim YS, Kang SS, Jeon SJ, Son KH, Lee SM: Protective effect of baicalin against carbon tetrachloride-induced acute hepatic injury in mice. J Pharmacol Sci. 2008 Jan;106(1):136-43. Epub 2008 Jan 11.

The mRNA and protein expression levels of inducible nitric oxide synthase and heme oxygenase-1 increased significantly at 24 h after the CCl (4) treatment.
3(0,0,0,3) Details
15496496 Aleksunes LM, Slitt AM, Cherrington NJ, Thibodeau MS, Klaassen CD, Manautou JE: Differential expression of mouse hepatic transporter genes in response to acetaminophen and carbon tetrachloride. Toxicol Sci. 2005 Jan;83(1):44-52. Epub 2004 Oct 20.

Heme oxygenase-1 (Ho-1), NAD (P) H quinone oxidoreductase-1 (Nqo1), organic anion-transporting polypeptides (Oatp1a1, 1a4 and 1b2), sodium/taurocholate-cotransporting polypeptide (Ntcp), and multidrug resistance-associated protein (Mrp 1-6) mRNA levels in liver were determined using the branched DNA signal amplification assay.
2(0,0,0,2) Details
19836219 Quan J, Yin X, Xu H: Boschniakia rossica prevents the carbon tetrachloride-induced hepatotoxicity in rat. Exp Toxicol Pathol. 2009 Oct 14.

Interestingly, the protein expression of heme oxygenase-1 (HO-1) was further elevated by BRE treatment, which was markedly increased after CCl (4) challenge.
2(0,0,0,2) Details
17229879 Bolognesi M, Sacerdoti D, Piva A, Di Pascoli M, Zampieri F, Quarta S, Motterlini R, Angeli P, Merkel C, Gatta A: Carbon monoxide-mediated activation of large-conductance calcium-activated potassium channels contributes to mesenteric vasodilatation in cirrhotic rats. J Pharmacol Exp Ther. 2007 Apr;321(1):187-94. Epub 2007 Jan 17.


In pressurized mesenteric arteries (diameter, 170-350 microm) of ascitic cirrhotic rats, we evaluated the effect of inhibition of BK (Ca), HO, and guanylyl-cyclase on dilatation induced by acetylcholine and by exogenous CO; and HO-1 and BK (Ca) subunit protein expression.
2(0,0,0,2) Details
18984026 Hwang YP, Choi JH, Jeong HG: Protective effect of the Aralia continentalis root extract against carbon tetrachloride-induced hepatotoxicity in mice. Food Chem Toxicol. 2009 Jan;47(1):75-81. Epub 2008 Oct 17.

Heme oxygenase-1 (HO-1) is known to be induced by oxidative stress and to confer protection against oxidative tissue injuries.
2(0,0,0,2) Details
17610505 Zhang L, Wan J, Li H, Wu P, Jin S, Zhou X, Yuan P, Xiong W, Li Y, Ye D: Protective effects of BML-111, a lipoxin A (4) receptor agonist, on carbon tetrachloride-induced liver injury in mice. Hepatol Res. 2007 Nov;37(11):948-56. Epub 2007 Jul 4.

Most interestingly, BML-111 markedly upregulated hepatic heme oxygenase-1 (HO-1) expression in CCl (4)-treated mice, which might provide antioxidative activities in the liver.
1(0,0,0,1) Details
18706400 Liu J, Wu Q, Lu YF, Pi J: New insights into generalized hepatoprotective effects of oleanolic acid: key roles of metallothionein and Nrf2 induction. Biochem Pharmacol. 2008 Oct 1;76(7):922-8. Epub 2008 Jul 23.

Oleanolic acid (OA) is a natural triperpenoid that protects against a variety of hepatotoxicants such as carbon tetrachloride, cadmium, acetaminophen, and bromobenzene.
OA treatment dramatically increased expression of hepatic metallothionein (Mt), and increased the expression of the nuclear factor E2-related factor 2 (Nrf2), NAD (P) H:quinone oxidoreductase 1 (Nqo1), heme oxygenase-1 (Hmox1), and glutamate-cysteine ligases (Gclc and Gclm).
1(0,0,0,1) Details
18078705 Randle LE, Goldring CE, Benson CA, Metcalfe PN, Kitteringham NR, Park BK, Williams DP: Investigation of the effect of a panel of model hepatotoxins on the Nrf2-Keap1 defence response pathway in CD-1 mice. Toxicology. 2008 Jan 20;243(3):249-60. Epub 2007 Oct 23.

Treatment with APAP for 1h caused a significant increase in the levels of haem oxygenase-1 (HO-1; 2.85-fold) and glutamate cysteine ligase (GCLC; 1.62-fold) mRNA.
Here, we have investigated, in vivo, whether the ability of four murine hepatotoxins, paracetamol, bromobenzene (BB), carbon tetrachloride (CCl4) and furosemide (FS) to deplete hepatic glutathione (GSH) is related to induction of hepatic Nrf2 nuclear translocation and Nrf2-dependent gene expression.
1(0,0,0,1) Details