Influence of selenium treatment on the acute toxicity of dibutyltin dichloride in rats

Lemke, M.; Görl, N.; Berg, Alan M.; Weber, Heike; Hennighausen, G.; Merkord, Jutta

doi:10.1159/000094666

Cited by 7 publications

(4 citation statements)

References 31 publications

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“…The major factors regulating GSH biosynthesis are the availability of cysteine [34]–[36]. Oxidative stress has been demonstrated to play an important role in the pathogenesis and progression of pancreatitis and also contributes to the development of pancreatic fibrosis [37]–[44]. Our current study showed that L-cysteine reduced the levels of MDA+4-HNE and enhanced the content of GSH in pancreatic tissues and PSCs, indicating its antioxidant effect which would ameliorate pancreatic fibrosis.…”

Section: Discussionsupporting

confidence: 54%

L-Cysteine Administration Attenuates Pancreatic Fibrosis Induced by TNBS in Rats by Inhibiting the Activation of Pancreatic Stellate Cell

Yang

Shen

et al. 2012

PLoS ONE

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Background and AimsRecent studies have shown that activated pancreatic stellate cells (PSCs) play a major role in pancreatic fibrogenesis. We aimed to study the effect of L-cysteine administration on fibrosis in chronic pancreatitis (CP) induced by trinitrobenzene sulfonic acid (TNBS) in rats and on the function of cultured PSCs.MethodsCP was induced by TNBS infusion into rat pancreatic ducts. L-cysteine was administrated for the duration of the experiment. Histological analysis and the contents of hydroxyproline were used to evaluate pancreatic damage and fibrosis. Immunohistochemical analysis of α-SMA in the pancreas was performed to detect the activation of PSCs in vivo. The collagen deposition related proteins and cytokines were determined by western blot analysis. DNA synthesis of cultured PSCs was evaluated by BrdU incorporation. We also evaluated the effect of L-cysteine on the cell cycle and cell activation by flow cytometry and immunocytochemistry. The expression of PDGFRβ, TGFβRII, collagen 1α1 and α-SMA of PSCs treated with different concentrations of L-cysteine was determined by western blot. Parameters of oxidant stress were evaluated in vitro and in vivo. Nrf2, NQO1, HO-1, IL-1β expression were evaluated in pancreas tissues by qRT-PCR.ResultsThe inhibition of pancreatic fibrosis by L-cysteine was confirmed by histological observation and hydroxyproline assay. α-SMA, TIMP1, IL-1β and TGF-β1 production decreased compared with the untreated group along with an increase in MMP2 production. L-cysteine suppressed the proliferation and extracellular matrix production of PSCs through down-regulating of PDGFRβ and TGFβRII. Concentrations of MDA+4-HNE were decreased by L-cysteine administration along with an increase in GSH levels both in tissues and cells. In addition, L-cysteine increased the mRNA expression of Nrf2, NQO1 and HO-1 and reduced the expression of IL-1β in L-cysteine treated group when compared with control group.ConclusionL-cysteine treatment attenuated pancreatic fibrosis in chronic pancreatitis in rats.

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Section: Discussionsupporting

confidence: 54%

L-Cysteine Administration Attenuates Pancreatic Fibrosis Induced by TNBS in Rats by Inhibiting the Activation of Pancreatic Stellate Cell

Yang

Shen

et al. 2012

PLoS ONE

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“…2)), as has been reported before (Lemke et al, 2006[15]). Moreover, it cannot be excluded that selenium forms unknown complexes with DBTC, which are not measurable by atomic absorption spectrometry.…”

Section: Discussionsupporting

confidence: 81%

“…In former studies we described the diminution by combined intravenous and oral selenium treatment on bile duct-, pancreas-, liver- and thymus lesions in rats after DBTC application (Lemke et al, 2006[15]). These results favoured the decreasing effects of selenium on oxidative stress, monitored by MDA levels, as an important mechanism in scope of DBTC-induced pancreatitis.…”

Section: Discussionmentioning

confidence: 99%

Influence of daily oral prophylactic selenium treatment on the dibutyltin dichloride (DBTC)-induced pancreatitis in rats

Merkord

Görl

Lemke

et al. 2017

EXCLI Journal; 16:Doc89; ISSN 1611-2156

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“…Mountains of research have been reported that DBTs are hepatotoxic [ 28 , 29 ]. Our research showed that HL7702 cells were damaged by DBTD at concentrations higher than 0.5 μmol/L, which was confirmed by increased ALT and AST activities in the culture media and an abnormally changed cell morphology ( Table 1 , Figure 2 ).…”

Section: Discussionmentioning

confidence: 99%

Effect of Dibutyltin Dilaurate on Triglyceride Metabolism through the Inhibition of the mTOR Pathway in Human HL7702 Liver Cells

Qiao

Mai

et al. 2018

Molecules

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Dibutyltin dilaurate (DBTD) has multiple applications in daily life. However, DBTD is easily deposited in the liver and affects liver functions. This study was designed to explore the effects of DBTD on triglyceride metabolism in human normal hepatocyte HL7702 cells. Our results showed that the intracellular fat contents were dose-dependently decreased by DBTD. The expression of lipolysis genes and proteins were elevated while the lipogenesis genes and proteins were diminished by DBTD. The phosphorylation levels of ribosomal S6 kinase 1 were reduced by both rapamycin and DBTD, indicating that the mTOR pathway was suppressed possibly. The decreased sterol regulatory element-binding protein 1C (SREBP1C) transcription levels, as well as the increased peroxisome proliferator-activated receptor alpha (PPARα) transcription levels, caused by rapamycin and DBTD corresponded to the inactive mTOR pathway. In conclusion, it was possible that DBTD reduced the intracellular triglyceride through depressing the mTOR pathway and affecting its downstream transcription factors.

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Influence of selenium treatment on the acute toxicity of dibutyltin dichloride in rats

Cited by 7 publications

References 31 publications

L-Cysteine Administration Attenuates Pancreatic Fibrosis Induced by TNBS in Rats by Inhibiting the Activation of Pancreatic Stellate Cell

L-Cysteine Administration Attenuates Pancreatic Fibrosis Induced by TNBS in Rats by Inhibiting the Activation of Pancreatic Stellate Cell

Influence of daily oral prophylactic selenium treatment on the dibutyltin dichloride (DBTC)-induced pancreatitis in rats

Effect of Dibutyltin Dilaurate on Triglyceride Metabolism through the Inhibition of the mTOR Pathway in Human HL7702 Liver Cells

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