Protective Effect of Diethyldithiocarbamate Pretreatment on Chromium(VI)-Induced Cytotoxicity and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes.

Susa, Nobuyuki; Ueno, Shunji; Furukawa, Yoshinori

doi:10.1292/jvms.60.71

Cited by 8 publications

(1 citation statement)

References 40 publications

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“…Pretreatment with DDTC completely prevented lipid peroxidation induced by CCl 4 (Figures 5a and b). 25,26 which can explain the decrease of basal lipid peroxidation. As a consequence, inhibition of CCl 4 -induced lipid peroxidation by 37% may not only result from CYP2E1 inhibition but also from the other properties of DDTC.…”

Section: Prevention Of CCL 4 -Induced Early Toxicity With Ddtcmentioning

confidence: 97%

Carbon tetrachloride-mediated lipid peroxidation induces early mitochondrial alterations in mouse liver

Knockaert

Berson

Ribault

et al. 2012

Laboratory Investigation

102

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Although carbon tetrachloride (CCl 4 )-induced acute and chronic hepatotoxicity have been extensively studied, little is known about the very early in vivo effects of this organic solvent on oxidative stress and mitochondrial function. In this study, mice were treated with CCl 4 (1.5 ml/kg ie 2.38 g/kg) and parameters related to liver damage, lipid peroxidation, stress/defense and mitochondria were studied 3 h later. Some CCl 4 -intoxicated mice were also pretreated with the cytochrome P450 2E1 inhibitor diethyldithiocarbamate or the antioxidants Trolox C and dehydroepiandrosterone. CCl 4 induced a moderate elevation of aminotransferases, swelling of centrilobular hepatocytes, lipid peroxidation, reduction of cytochrome P4502E1 mRNA levels and a massive increase in mRNA expression of heme oxygenase-1 and heat shock protein 70. Moreover, CCl 4 intoxication induced a severe decrease of mitochondrial respiratory chain complex IV activity, mitochondrial DNA depletion and damage as well as ultrastructural alterations. Whereas DDTC totally or partially prevented all these hepatic toxic events, both antioxidants protected only against liver lipid peroxidation and mitochondrial damage. Taken together, our results suggest that lipid peroxidation is primarily implicated in CCl 4 -induced early mitochondrial injury. However, lipid peroxidation-independent mechanisms seem to be involved in CCl 4 -induced early hepatocyte swelling and changes in expression of stress/defense-related genes. Antioxidant therapy may not be an efficient strategy to block early liver damage after CCl 4 intoxication.

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Section: Prevention Of CCL 4 -Induced Early Toxicity With Ddtcmentioning

confidence: 97%

Carbon tetrachloride-mediated lipid peroxidation induces early mitochondrial alterations in mouse liver

Knockaert

Berson

Ribault

et al. 2012

Laboratory Investigation

102

View full text Add to dashboard Cite

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Inhibitory effect of SJSZ glycoprotein (38 kDa) on expression of heat shock protein 27 and 70 in chromium (VI)-treated hepatocytes

Liu

Lim

2011

Mol Cell Biochem

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Chromium (VI) is as an extremely toxic chemical substance, and is also an internationally recognized human carcinogen. The principal objective of this study was to determine whether or not Styrax japonica Siebold et al. Zuccarini (SJSZ) glycoprotein prevents hepatocarcinogenesis in chromium-treated BNL CL.2 cells and ICR mice. Firstly, it was evaluated that SJSZ glycoprotein has strong antioxidant character and scavenges radicals. In an effort to assess the chemopreventive effects of SJSZ glycoprotein on hepatocarcinogenesis, ICR mice were intraperitoneally injected with chromium (10 mg/kg, BW) for 8 weeks. After sacrifice, we evaluated indicators of liver tissue damage [the activities of lactate dehydrogenase (LDH) and alanine aminotransferase (ALT), and thiobarbituric acid-reactive substances (TBARS)], antioxidative enzymes [activities of superoxide dismutase (SOD), catalase (CAT) and gluthathione peroxidase (GPx)], and initiating hepatocarcinogenic indicator [heat shock protein (HSP) 27 and 70] and protein kinase C (PKC), p38 MAPK and PCNA via biochemical methods and immunoblot analysis. The results obtained from this study demonstrated that the SJSZ glycoprotein (50 μg/ml) inhibited the production of intracellular ROS in BNL CL.2 cells. In addition, the SJSZ glycoprotein (10 mg/kg, BW) attenuated the levels of LDH, ALT, and TBARS, whereas it increased antioxidative enzymes in mouse serum. SJSZ glycoprotein attenuated the activity of HSP27, HSP70, PKC, MAPKs, and PCNA in BNL CL.2 cells and liver tissue. Taken together, our results indicate that SJSZ glycoprotein might be have a potent preventive effect against hepatocarcinogenesis induced by oxidative stress.

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Inhibitory effect of Styrax Japonica Siebold et al. Zuccarini glycoprotein (38 kDa) on interleukin-1β and induction proteins in chromium(VI)-treated BNL CL.2 cells

Liu

Lim

2012

Mol Cell Biochem

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Chromium(VI) [Cr(VI)] induces chronic inflammation in hepatocytes. Inflammation has been shown to play an important role in tumorigenesis, tumor progression, and metastasis. To examine the effects of the Styrax Japonica Siebold et al. Zuccarini (SJSZ) glycoprotein on inflammation in BNL CL.2 cells, we evaluated the activities of c-Jun NH(2)-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), nuclear factor (NF)-κB (p50 and p65), and inflammation-related factors [cyclooxygenase (COX)-2, inducible nitric oxide syntheses (iNOS) and interleukin (IL)-1β] in Cr-induced BNL CL.2 cells using immunoblot analysis and RT-PCR. We also used two-dimensional gel electrophoresis (2-DE) to compare between treatments. To determine which proteins are induced by Cr(VI), we evaluated total protein lysates using 2-DE. After Cr(VI) treatment, total protein lysates were prepared and resolved by 2-DE. The results obtained from this study demonstrated that the SJSZ glycoprotein (50 μg/ml) inhibits expression of JNK, ERK, NF-κB, and the expression of COX-2, iNOS, and IL-1β. Moreover, the results obtained from 2DE showed that four proteins out of nine proteins were relatively expressed strongly, while the rest of them were relatively appeared weakly on the gel. Taken together, these data indicate that the SJSZ glycoprotein prevents expression of COX-2, iNOS, and IL-1β by blocking NF-κB and MAPKs in Cr(VI)-induced BNL CL.2 cells.

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Protective Effect of Diethyldithiocarbamate Pretreatment on Chromium(VI)-Induced Cytotoxicity and Lipid Peroxidation in Primary Cultures of Rat Hepatocytes.

Cited by 8 publications

References 40 publications

Carbon tetrachloride-mediated lipid peroxidation induces early mitochondrial alterations in mouse liver

Carbon tetrachloride-mediated lipid peroxidation induces early mitochondrial alterations in mouse liver

Inhibitory effect of SJSZ glycoprotein (38 kDa) on expression of heat shock protein 27 and 70 in chromium (VI)-treated hepatocytes

Inhibitory effect of Styrax Japonica Siebold et al. Zuccarini glycoprotein (38 kDa) on interleukin-1β and induction proteins in chromium(VI)-treated BNL CL.2 cells

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