INT38856

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Context Info
Confidence 0.69
First Reported 1981
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 24
Total Number 25
Disease Relevance 9.55
Pain Relevance 1.62

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

extracellular space (Ccl4) extracellular region (Ccl4)
Anatomy Link Frequency
liver 3
body 2
band 1
hepatic parenchyma 1
Ccl4 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
chemokine 29 100.00 Very High Very High Very High
fibrosis 11 99.36 Very High Very High Very High
agonist 1 96.60 Very High Very High Very High
alcohol 66 96.32 Very High Very High Very High
Paracetamol 9 95.12 Very High Very High Very High
Glutamate 8 92.24 High High
Inflammation 87 86.28 High High
antagonist 9 84.36 Quite High
anesthesia 16 84.24 Quite High
tolerance 2 76.56 Quite High
Disease Link Frequency Relevance Heat
Body Weight 201 100.00 Very High Very High Very High
Hepatotoxicity 110 99.96 Very High Very High Very High
Poisoning 163 99.74 Very High Very High Very High
Cirrhosis 30 99.64 Very High Very High Very High
Fibrosis 9 99.36 Very High Very High Very High
Hypoxia 6 99.22 Very High Very High Very High
Apoptosis 133 99.04 Very High Very High Very High
Hepatitis Virus Infection 3 97.84 Very High Very High Very High
Stress 139 96.96 Very High Very High Very High
Renal Disease 14 96.72 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Extensive evidence demonstrates that as a result of the metabolic activation of CCl4, •CCl4 and •Cl, are formed which initiate lipid peroxidation process.
Positive_regulation (activation) of CCl4
1) Confidence 0.69 Published 2005 Journal BMC Pharmacol Section Body Doc Link PMC549532 Disease Relevance 0.43 Pain Relevance 0
Extensive evidence demonstrates that as a result of the metabolic activation of CCl4, •CCl4 and •Cl, are formed which initiate lipid peroxidation process.
Positive_regulation (activation) of CCl4
2) Confidence 0.69 Published 2005 Journal BMC Pharmacol Section Body Doc Link PMC549532 Disease Relevance 0.43 Pain Relevance 0
The probable mechanism by which the root extract exerts its protective action against CCl4-induced hepatocellular metabolic alterations could be by the stimulation of hepatic regeneration through an improved synthesis of protein or interference with the microsomal activation of CCl4 and/or its accelerated detoxification and excretion.
Positive_regulation (activation) of CCl4
3) Confidence 0.68 Published 2010 Journal Journal of Pharmacy and Bioallied Sciences Section Body Doc Link PMC2996063 Disease Relevance 0.24 Pain Relevance 0
The activation of CCl4 to ·CCl3 is caused via the cytochrom P450 system in the liver [4, 5].
Positive_regulation (activation) of CCl4 in liver
4) Confidence 0.67 Published 2008 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2266062 Disease Relevance 0.42 Pain Relevance 0.07
Therefore, it seems unlikely that octacosanol administered orally to CCl4-intoxicated rats at 6 h after intoxication affects the activation of CCl4 to ·CCl3 and CCl3O2· via the cytochrome P450 system followed by the covalent binding of ·CCl3 to membrane lipids and lipid peroxidation mediated by ·CCl3 and CCl3O2· in the liver.
Positive_regulation (activation) of CCl4 in liver associated with poisoning
5) Confidence 0.67 Published 2008 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2266062 Disease Relevance 0.60 Pain Relevance 0.03
It is also known that when rats are intoxicated with CCl4 (5 ml/kg BW, i.p.), the activation of CCl4 to ·CCl3 and CCl3O2·, the covalent binding of ·CCl3 to membrane lipids and proteins, and the hydrogen abstraction from polyunsaturated fatty acids by the CCl3O2· and the ·CCl3 to initiate lipid peroxidation terminate within a few hours after intoxication [29, 30].
Positive_regulation (activation) of CCl4 associated with body weight and poisoning
6) Confidence 0.67 Published 2008 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2266062 Disease Relevance 0.42 Pain Relevance 0.03
According to the present views of the initial developmental process of CCl4-induced hepatotoxicity, the process is dominated by factors such as CCl4 activation to trichloromethyl radical (·CCl3) and trichloromethyl peroxy radical (CCl3O2·), the covalent binding of ·CCl3 to membrane lipids and proteins, and the hydrogen abstraction from polyunsaturated fatty acids by the CCl3O2· and the ·CCl3 to initiate lipid peroxidation [4, 5].
Positive_regulation (activation) of CCl4 associated with hepatotoxicity
7) Confidence 0.67 Published 2008 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2266062 Disease Relevance 0.39 Pain Relevance 0
DNP-induced hypoxia resulting in an accelerated metabolic activation of CCl4 presumably accounts for the interaction between DNP and CCl4.
Positive_regulation (activation) of CCl4 associated with hypoxia
8) Confidence 0.61 Published 1981 Journal Toxicol. Lett. Section Abstract Doc Link 7314128 Disease Relevance 0.17 Pain Relevance 0.14
Studies done with Ginseng showed that the antioxidant property of ginsenosides contributes to protection against CCl4 induced hepatotoxicity in rats [28].
Positive_regulation (induced) of CCl4 associated with hepatotoxicity
9) Confidence 0.49 Published 2005 Journal BMC Pharmacol Section Body Doc Link PMC549532 Disease Relevance 0.55 Pain Relevance 0
Also, CCl4 showed a significant increase in serum sialic acid; nitrite levels; total LDH activity and hepatic malondialdehyde (LPO) level compared to normal control value.
Positive_regulation (increase) of CCl4
10) Confidence 0.45 Published 2010 Journal Scientia Pharmaceutica Section Body Doc Link PMC3007612 Disease Relevance 0 Pain Relevance 0
Increased activation of Bax and Bid in CCl4 treated rats indicates apoptosis is more in these rats.
Positive_regulation (activation) of CCl4 associated with apoptosis
11) Confidence 0.43 Published 2010 Journal BMC Pharmacol Section Body Doc Link PMC2967507 Disease Relevance 0.88 Pain Relevance 0.06
The levels of oxidized glutathione (GSSG) increased by 73% in CCl4 treated rats when compared to controls.
Positive_regulation (increased) of CCl4
12) Confidence 0.43 Published 2010 Journal BMC Pharmacol Section Body Doc Link PMC2967507 Disease Relevance 0.09 Pain Relevance 0
Mitochondrial cytochrome C, detected as a single band of molecular mass (14 kDa) was increased in the whole cell lysate of CCl4 treated rats, compared to controls (Figure 7).
Positive_regulation (increased) of CCl4 in band
13) Confidence 0.43 Published 2010 Journal BMC Pharmacol Section Body Doc Link PMC2967507 Disease Relevance 0.64 Pain Relevance 0.04
Group 4: Received natansnin (10 mg/kg body wt) in 0.5 ml of mineral oil orally for a period of 8 days and then CCl4 (4 g/kg body wt) was given and sacrificed after 24 h.
Positive_regulation (sacrificed) of CCl4 in body
14) Confidence 0.43 Published 2010 Journal BMC Pharmacol Section Body Doc Link PMC2967507 Disease Relevance 0.16 Pain Relevance 0
Immuno blot analysis of pro caspase-3 (17 kDa) and active caspase-3 (32 kDa) increased in CCl4 treated rats and densitometric analysis of this protein is also shown in Figure 7.
Positive_regulation (increased) of CCl4
15) Confidence 0.43 Published 2010 Journal BMC Pharmacol Section Body Doc Link PMC2967507 Disease Relevance 0.56 Pain Relevance 0.04
Group 5: Received natansnin (20 mg/kg body wt) in 0.5 ml of mineral oil orally for a period of 8 days and then CCl4 (4 g/kg body wt) was given and sacrificed after 24 h.


Positive_regulation (sacrificed) of CCl4 in body
16) Confidence 0.43 Published 2010 Journal BMC Pharmacol Section Body Doc Link PMC2967507 Disease Relevance 0.17 Pain Relevance 0
Both the doses of HDN also attenuated the CCl4-induced elevated levels of total bilirubin (control = 0.184 mg/dl).


Positive_regulation (induced) of CCl4
17) Confidence 0.43 Published 2005 Journal BMC Pharmacol Section Body Doc Link PMC549532 Disease Relevance 0.54 Pain Relevance 0.07
It is also known that when rats are intoxicated with CCl4 (5 ml/kg BW, i.p.), the activation of CCl4 to ·CCl3 and CCl3O2·, the covalent binding of ·CCl3 to membrane lipids and proteins, and the hydrogen abstraction from polyunsaturated fatty acids by the CCl3O2· and the ·CCl3 to initiate lipid peroxidation terminate within a few hours after intoxication [29, 30].
Positive_regulation (activation) of CCl4 associated with body weight and poisoning
18) Confidence 0.42 Published 2008 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2266062 Disease Relevance 0.42 Pain Relevance 0.04
Naik and Panda [17] have observed a decreased serum level of total protein in CCl4 induced hepatotoxicity in rats.
Positive_regulation (induced) of CCl4 associated with hepatotoxicity
19) Confidence 0.42 Published 2010 Journal Scientia Pharmaceutica Section Body Doc Link PMC3007612 Disease Relevance 0.20 Pain Relevance 0
Moreover, benoxaprofen and indomethacin but not flunoxaprofen induced a significant increase of some serum liver enzymes in CCl4 poisoned rats.
Positive_regulation (increase) of CCl4 in liver
20) Confidence 0.41 Published 1985 Journal Drugs Exp Clin Res Section Abstract Doc Link 3836872 Disease Relevance 0.15 Pain Relevance 0.19

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