Cytotoxicity of millimolar concentrations of ethanol on HepG2 human tumor cell line compared to normal rat hepatocytes in vitro

Castañeda, Francisco; Kinne, Rolf K. H.

doi:10.1007/s004320000119

Cited by 26 publications

(24 citation statements)

References 30 publications

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“…These results indicated clearly that sulfation of ethanol may occur in cells under the metabolic setting. Since previous studies indicated that ethanol may exert cytotoxicity, 34,35) cell viability assay based on trypan blue exclusion or MTT reduction was performed to verify the viability of HepG2 cells used in the metabolic labeling experiments. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Ethanol Sulfation by the Human Cytosolic Sulfotransferases: A Systematic Analysis

Kurogi

Davidson

Mohammed

et al. 2012

Biological & Pharmaceutical Bulletin

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Section: Resultsmentioning

confidence: 99%

Ethanol Sulfation by the Human Cytosolic Sulfotransferases: A Systematic Analysis

Kurogi

Davidson

Mohammed

et al. 2012

Biological & Pharmaceutical Bulletin

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“…96 Furthermore, low ethanol concentrations (1 mmol) inhibit cell proliferation and increase apoptosis more strongly in hepatocarcinoma cells than in normal hepatocytes. 97 Ethanol injection can lengthen survival in patients with hepatocellular carcinoma. 98 Carcinogens are cytotoxic to certain cancer cells.…”

Section: Carcinogens As Anticancer Drugsmentioning

confidence: 99%

Carcinogenesis, cancer therapy and chemoprevention

Blagosklonny

2005

Cell Death Differ

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Carcinogenesis and cancer therapy are two sides of the same coin, such that the same cytotoxic agent can cause cancer and be used to treat cancer. This review links carcinogenesis, chemoprevention and cancer therapy in one process driven by cytotoxic agents (carcinoagents) that select either for or against cells with oncogenic alterations. By unifying therapy and cancer promotion and by distinguishing nononcogenic and oncogenic mechanisms of resistance, I discuss anticancer-and chemopreventive agent-induced carcinogenesis and tumor progression and, vice versa, carcinogens as anticancer drugs, anticancer drugs as chemopreventive agents and exploiting oncogene-addiction and drug resistance for chemoprevention and cancer therapy.

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“…YP1 staining performed in gastric glands, pieces of dissected skin, and isolated retina samples from mice and rats has resulted in the identification of a clear distinction between live and apoptotic cells (Ito et al 2010;Kohler et al 2010;Liao and Puro 2006). Other investigators have cultured hepatocyte spheroids and convincingly determined apoptotic cells using YP1 (Castañeda and Kinne 2000;Higashiyama et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…In a prior investigation, YP1 was used successfully to assess the viability of isolated pancreatic islets immediately after harvesting from deceased organ donors (Boffa et al 2005). In addition, at least 2 prior studies have used YP1 in hepatocyte spheroids grown in culture (Castañeda and Kinne 2000;Higashiyama et al 2003) and have demonstrated that this dye can be used in liver cells. Based on these findings, we postulated that YP1 could also be used in human liver tissues obtained after RFA, and would thus allow an early assessment of apoptosis leading to cellular death.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of YO-PRO-1 as an early marker of apoptosis following radiofrequency ablation of colon cancer liver metastases

et al. 2013

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Radiofrequency (RF) ablation (RFA) is a minimally invasive treatment for colorectal-cancer liver metastases (CLM) in selected nonsurgical patients. Unlike surgical resection, RFA is not followed by routine pathological examination of the target tumor and the surrounding liver tissue. The aim of this study was the evaluation of apoptotic events after RFA. Specifically, we evaluated YO-PRO-1 (YP1), a green fluorescent DNA marker for cells with compromised plasma membrane, as a potential, early marker of cell death. YP1 was applied on liver tissue adherent on the RF electrode used for CLM ablation, as well as on biopsy samples from the center and the margin of the ablation zone as depicted by dynamic CT immediately after RFA. Normal pig and mouse liver tissues were used for comparison. The same samples were also immunostained for fragmented DNA (TUN-EL assay) and for active mitochondria (anti-OxPhos antibody). YP1 was also used simultaneously with propidium iodine (PI) to stain mouse liver and samples from ablated CLM. Following RFA of human CLM, more than 90 % of cells were positive for YP1. In nonablated, dissected pig and mouse liver however, we found similar YP1 signals (93.1 % and 65 %, respectively). In samples of intact mouse liver parenchyma, there was a significantly smaller proportion of YP1 positive cells (22.7 %). YP1 and PI staining was similar for ablated CLM. However in dissected normal mouse liver there was initial YP1 positivity and complete absence of the PI signal and only later there was PI signal. Conclusion: This is the first time that YP1 was applied in liver parenchymal tissue (rather than cell culture). The results suggest that YP1 is a very sensitive marker of early cellular events reflecting an early and widespread plasma membrane injury that allows YP1 penetration into the cells.

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Cytotoxicity of millimolar concentrations of ethanol on HepG2 human tumor cell line compared to normal rat hepatocytes in vitro

Cited by 26 publications

References 30 publications

Ethanol Sulfation by the Human Cytosolic Sulfotransferases: A Systematic Analysis

Ethanol Sulfation by the Human Cytosolic Sulfotransferases: A Systematic Analysis

Carcinogenesis, cancer therapy and chemoprevention

Evaluation of YO-PRO-1 as an early marker of apoptosis following radiofrequency ablation of colon cancer liver metastases

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