Effect of regeneration and hyperplasia on levels of DNA base oxidation in rat liver

Murkofsky, Rachel L.; Glover, Sarah E.; Miller, Richard T.; Popp, James A.; Cattley, Russell C.

doi:10.1016/0304-3835(93)90074-j

Cited by 5 publications

(2 citation statements)

References 21 publications

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“…There was also a remarkable shortening of the cell cycle in the hepatocytes of PB-treated animals. In agreement with this result, Murkofsky et al [37] reported that PB treatment induced cell proliferation in the rat liver. A study by Kinoshita et al [38] revealed correlative changes in oxidative stress, proliferation, apoptosis, and DNA damage and repair, which occur in the rat liver during continuous PB exposure.…”

Section: Discussionsupporting

confidence: 77%

An autoradiographic study of cellular proliferaton, DNA synthesis and cell cycle variability in the rat liver caused by phenobarbital-induced oxidative stress: The protective role of melatonin

El‐Sokkary¹

2007

Cellular and Molecular Biology Letters

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Abstract:The protective effect of melatonin against phenobarbital-induced oxidative stress in the rat liver was measured based on lipid peroxidation levels (malondialedyde and 4-hydroxyalkenals). Cellular proliferation, DNA synthesis and cell cycle duration were quantitated by the incorporation of 3 H-thymidine, detected by autoradiography, into newly synthesized DNA. Two experiments were carried out in this study, each on four equal-sized groups of male rats (control, melatonin [10 mg/kg], phenobabital [20 mg/kg] and phenobarbital plus melatonin). Experiment I was designed to study the proliferative activity and rate of DNA synthesis, and measure the levels of lipid peroxidation, while experiment II was for cell cycle time determination. Relative to the controls, the phenobarbital-treated rats showed a significant increase (P < 0.01) in the lipid peroxidation levels (30.7%), labelling index (69.4%) and rate of DNA synthesis (37.8%), and a decrease in the cell cycle time. Administering melatonin to the phenobarbital-treated rats significantly reduced (P < 0.01) the lipid peroxidation levels (23.5%), labelling index (38.2%) and rate of DNA synthesis (29.0%), and increased the cell cycle time. These results seem to indicate that the stimulatory effect of phenobarbital on the oxidized lipids, proliferative activity, kinetics of DNA synthesis and cell cycle time alteration in the liver may be one of the mechanisms by which the non-genotoxic mitogen induces its carcinogenic action. Furthermore, melatonin displayed powerful protection against the toxic effect of phenobarbital.

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Section: Discussionsupporting

confidence: 77%

An autoradiographic study of cellular proliferaton, DNA synthesis and cell cycle variability in the rat liver caused by phenobarbital-induced oxidative stress: The protective role of melatonin

El‐Sokkary¹

2007

Cellular and Molecular Biology Letters

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“…The short-term increase in cell proliferation observed here in ETBE-treated rat livers indicates that the peak of 8-OHdG generation, followed by cell cycle arrest and induction of apoptosis, is likely to occur at day 14, as we reported previously 5 , 8 . Early elevation of cell proliferation as an acute response to treatment with a non-genotoxic chemical was previously demonstrated with PB 10 , 13 , 14 . Thus, PB administered to F344 rats at a dose of 500 ppm was shown to induce time-dependent elevation of cell proliferation starting at day 1 or 2 and reaching its peak at day 6, followed by a decrease at day 8, which was associated with induction of 8-OHdG formation and apoptosis 10 .…”

Section: Discussionmentioning

confidence: 72%

Induction of cell proliferation in the rat liver by the short-term administration of ethyl <i>tertiary</i>-butyl ether

Kakehashi

Hagiwara²,

Imai³

et al. 2015

J Toxicol Pathol

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In the present study, in continuation of our previous experiment in order to investigate the mode of action (MOA) of ethyl tertiary-butyl ether (ETBE) hepatotumorigenicity in rats, we aimed to examine alterations in cell proliferation, that are induced by short-term administration of ETBE. F344 rats were administered ETBE at doses of 0, and 1,000 mg/kg body weight twice a day by gavage for 3, 10, 17 and 28 days. It was found that the previously observed significant increase of P450 total content and hydroxyl radical levels after 7 days of ETBE administration, and 8-OHdG formation at day 14, accompanied by accumulation of CYP2B1/2B2, CYP3A1/3A2, CYP2C6, CYP2E1 and CYP1A1 and downregulation of DNA oxoguanine glycosylase 1, was preceded by induction of cell proliferation at day 3. Furthermore, we observed an increase in regenerative cell proliferation as a result of ETBE treatment at day 28, followed by induction of cell cycle arrest and apoptosis by day 14. These results indicated that short-term administration of ETBE led to a significant early increase in cell proliferation activity associated with induction of oxidative stress, and to a regenerative cell proliferation as an adaptive response, which could contribute to the hepatotumorigenicity of ETBE in rats.

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Comparison of cell proliferation following partial hepatectomy in rats fed NIH-31 or semipurified AIN-76A diets: Effects of nucleic acid supplementation

et al. 1995

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Effect of regeneration and hyperplasia on levels of DNA base oxidation in rat liver

Cited by 5 publications

References 21 publications

An autoradiographic study of cellular proliferaton, DNA synthesis and cell cycle variability in the rat liver caused by phenobarbital-induced oxidative stress: The protective role of melatonin

An autoradiographic study of cellular proliferaton, DNA synthesis and cell cycle variability in the rat liver caused by phenobarbital-induced oxidative stress: The protective role of melatonin

Induction of cell proliferation in the rat liver by the short-term administration of ethyl <i>tertiary</i>-butyl ether

Comparison of cell proliferation following partial hepatectomy in rats fed NIH-31 or semipurified AIN-76A diets: Effects of nucleic acid supplementation

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