Effects of selenium supplementation on hepatocarcinogenesis in rats

Aquino, Therese M.; Porta, Eduardo A.; Sablan, Herbert M.; Dorado, Russell D.

doi:10.1080/01635588509513836

Cited by 12 publications

(5 citation statements)

References 38 publications

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“…The lack of preventive effect of selenium was observed whether it was given during initiation, during promotion or during the entire experiment. These negative results confirm and extend, therefore, those obtained in our previous study (10). We believe that the discrepancy between our findings and those previously reported by other investigators (2-7) is most likely due to the manner of conducting the experiments and analyzing the data.…”

Section: Discussionsupporting

confidence: 82%

Effects of dietary selenium on hepatic and renal tumorigenesis induced in rats by diethylnitrosamine

Dorado¹,

Porta²,

Aquino³

1985

Hepatology

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Seven groups of female Sprague-Dawley rats (approximately 200 gm initial body weight) were injected i.p. with a single subcarcinogenic dose of diethylnitrosamine (40 mg per kg body weight) between 8 to 10 hr after partial hepatectomy, and after a recovery period of 3 weeks (herein called induction stage) received 0.05% phenobarbital in the diet for the rest of the experiment (promotion stage). The rats were fed a 20% casein-based diet containing 0.16 ppm of selenium or the same diet supplemented with 4 or 6 ppm of selenium as sodium selenite. The effects of these three dietary regimens were tested when administered 9 to 11 days before and during induction, 1 week before and during promotion or during the entire experiment. Pair-feeding conditions were used to minimize influences due to differences in food intake and growth. Despite similarities in food intakes, the growth rates in groups receiving the 6 ppm-selenium diet during promotion or during the entire experiment were in general significantly lower than in rats fed the 4 ppm-selenium diet or the 0.16 ppm-selenium basal diet. Survival rates were also significantly reduced in rats fed the 4 and 6 ppm-selenium diets during promotion or during the entire experiment. In rats killed at the 19th week for interim assessment of the experiment's progress, the stereologically analyzed numerical and volumetric densities of hepatic premalignant hyperplastic nodules did not differ significantly between groups. All the remaining rats were killed at the 46th week.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 82%

Effects of dietary selenium on hepatic and renal tumorigenesis induced in rats by diethylnitrosamine

Dorado¹,

Porta²,

Aquino³

1985

Hepatology

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“…It is also known that dihydroferulic acid or dihydrosinaptic acid contained in an unpolished rice vinegar possesses a potent radical scavenging activity (26). It is possible that the effect of FBRA is mediated through the action of several trace elements, including selenium which is biotransformed to an organic form during the fermentation of brown rice and rice bran (27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

Preventive effect of fermented brown rice and rice bran on N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric carcinogenesis in rats

Tomita

Kuno²,

Yamada³

et al. 2008

Oncol Rep

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A number of possible preventive agents for cancers in different organs have been reported, however, little information is available regarding the effective agents for the development of gastric cancers. The rice components are known to be effective for the prevention of the development of cancers. Our group has demonstrated that fermented brown rice by Aspergillus Orzae (FBRA) has chemopreventive potentials in several organs. In this study, we investigated the modifying effects of FBRA exposed during the initiation or post-initiation phase of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis in rats. Five-weekold male ACI rats were divided into 7 groups. Groups 1-5 were given oral administration of MNNG (100 mg/l in distilled water) for 24 weeks starting at 6 weeks of age. Groups 2 and 3 were fed a diet containing 5 and 10% FBRA during the initiation phase, respectively, whereas groups 4 and 5 were fed these diets during the post-initiation phase. Group 6 was given a diet containing 10% FBRA throughout the experiment. Group 7 was kept on the basal diet alone and served as an untreated control. Rats were sacrificed at 52 weeks after the start, and the epithelium of the stomach was investigated in detail. Incidence and multiplicity of gastric proliferative lesions of group 1 (MNNG alone) were 61% and 1.67±1.57/ rat, respectively. Those of group 5 (25%, 0.35±0.67) which were given FBRA at a dose of 10% during the post-initiation phase were significantly less than those of group 1. Furthermore, the same group expressed a significantly decreased Ki67-labeling index in the non-lesional gastric epithelium when compared to that of group 1. These results indicate that FBRA inhibits MNNG-induced development of gastric tumors by administration during the post-initiation phase in rats. FBRA is regarded as a promising dietary agent for the prevention of human gastric cancer.

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“…Several studies have investigated the effect of Se on different phases of hepatocarcinogenesis using varying in vivo hepatocarcinogenesis protocols, initiating agents and tumor promoters. Two studies that used DEN as the initiator and phenobarbital (PB) as the promoting agent demonstrated that Se did not affect the induction of hyperplastic hepatic nodules or carcinomas when Se supplementation was given during either the initiation or promotion stages, or throughout the entire study (49,50). Milks et al (51) found that feeding higher levels of Se only during aflatoxin B 1 (AFB1) administration inhibited the subsequent development of altered hepatic foci.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dietary Selenium on the Promotion of Hepatocarcinogenesis by 3,3′, 4,4′-Tetrachlorobiphenyl and 2,2′, 4,4′, 5,5′-Hexachlorobiphenyl

Stemm

Tharappel²,

Lehmler³

et al. 2008

Exp Biol Med (Maywood)

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Polychlorinated biphenyls (PCBs) are persistent organic pollutants that have promoting activity in the liver. PCBs induce oxidative stress, which may influence carcinogenesis. Epidemiological studies strongly suggest an inverse relationship between dietary selenium (Se) and cancer. Despite evidence linking Se deficiency to hepatocellular carcinoma and liver necrosis, the underlying mechanisms for Se cancer protection in the liver remain to be determined. We examined the effect of dietary Se on the tumor promoting activities of two PCBs congeners, 3,3', 4,4'-tetrachlorobiphenyl (PCB-77) and 2,2', 4,4', 5,5'-hexachlorobiphenyl (PCB-153) using a 2-stage carcinogenesis model. An AIN-93 torula yeast-based purified diet containing 0.02 (deficient), 0.2 (adequate), or 2.0 mg (supplemental) selenium/kg diet was fed to Sprague-Dawley female rats starting ten days after administering a single dose of diethylnitrosamine (150 mg/kg). After being fed the selenium diets for 3 weeks, rats received four i.p. injections of either PCB-77 or PCB-153 (150 micromol/kg) administered every 14 days. The number of placental glutathione S-transferase (PGST)-positive foci per cm(3) and per liver among the PCB-77-treated rats was increased as the Se dietary level increased. Unlike PCB-77, rats receiving PCB-153 did not show the same Se dose-response effect; nevertheless, Se supplementation did not confer protection against foci development. However, the 2.0 ppm Se diet reduced the mean focal volume, indicating a possible protective effect by inhibiting progression of preneoplastic lesions into larger foci. Cell proliferation was not inhibited by Se in the liver of the PCB-treated groups. Se did not prevent the PCB-77-induced decrease of hepatic Se and associated reduction in glutathione peroxidase (GPx) activity. In contrast, thioredoxin reductase (TrxR) activity was not affected by the PCBs treatment or by Se supplementation. These findings indicate that Se does not inhibit the number of PGST-positive foci induced during promotion by PCBs, but that the size of the lesions may be inhibited. The effects of Se on altered hepatic foci do not correlate with its effects on GPx and TrxR.

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Effects of selenium supplementation on hepatocarcinogenesis in rats

Cited by 12 publications

References 38 publications

Effects of dietary selenium on hepatic and renal tumorigenesis induced in rats by diethylnitrosamine

Effects of dietary selenium on hepatic and renal tumorigenesis induced in rats by diethylnitrosamine

Preventive effect of fermented brown rice and rice bran on N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric carcinogenesis in rats

Effect of Dietary Selenium on the Promotion of Hepatocarcinogenesis by 3,3′, 4,4′-Tetrachlorobiphenyl and 2,2′, 4,4′, 5,5′-Hexachlorobiphenyl

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