Comparative study on pyruvate kinase activity‐reducing action of various promoters of hepatocarcinogenesis

Yanagi, Susumu; Sakamoto, Mitsuaki; Nakano, Tetsuya

doi:10.1002/ijc.2910370319

Cited by 7 publications

(2 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although Oleic and Lauric Acids induced mitotic aneuploidy during in vitro mutagenicity tests, both were considered inhibitors of mutagenicity (produced by positive controls, such (Elder 1987). Yanagi, Sakamoto, and Nakano (1986) noted that chemicals that enhanced formation of hyperplastic nodules in the rat liver also caused marked increases of pyruvate kinase (PK) activity. PK activity in rats was typically decreased during feeding of hepatic promoters and the extent of the decrease was inversely correlated with the doses.…”

Section: Genotoxicitymentioning

confidence: 99%

Final Report on the Safety Assessment of Sorbitan Caprylate, Sorbitan Cocoate, Sorbitan Diisostearate, Sorbitan Dioleate, Sorbitan Distearate, Sorbitan Isostearate, Sorbitan Olivate, Sorbitan Sesquiisostearate, Sorbitan Sesquistearate, and Sorbitan Triisostearate

Lanigan¹,

Yamarik²

2002

Int J Toxicol

View full text Add to dashboard Cite

Sorbitan fatty acid esters are mono-, di-, and triesters of fatty acids and sorbitol-derived hexitol anhydrides. They function as surfactants in cosmetic formulations. Previously, the Cosmetic Ingredient Review (CIR) Expert Panel had reviewed the safety of several of these sorbitan fatty acid esters (Sorbitan Laurate, Sorbitan Oleate, Sorbitan Palmitate, Sorbitan Sesquioleate, Sorbitan Stearate, Sorbitan Trioleate, and Sorbitan Tristearate). This safety assessment is an addendum to that report that includes Sorbitan Caprylate, Sorbitan Cocoate, Sorbitan Diisostearate, Sorbitan Dioleate, Sorbitan Distearate, Sorbitan Isostearate, Sorbitan Olivate, Sorbitan Sesquiisostearate, Sorbitan Sesquistearate, and Sorbitan Triisostearate. Although concentrations of these ingredients up to 25% have been reported to be used, most commonly they are used at less than 10%. These esters may be hydrolyzed to the fatty acid and anhydrides of Sorbitol. Fatty Acids are absorbed and metabolized. Sorbitan fatty acid esters were relatively nontoxic via ingestion in acute and long-term studies. They were generally minimal to mild skin irritants in animal studies, except that Sorbitan Isostearate applied to the skin was a moderate irritant in one rabbit study and when injected intradermally caused mild to severe irritation in guinea pigs. Sorbitan fatty acid esters did not sensitize guinea pigs. The fatty acid component, tested alone, typically caused only slight irritation and sensitization, and was not photosensitizing. Sorbitan fatty acid esters were not ocular irritants. Fatty acids are normal components of diet for which no data were available concerning reproductive or developmental toxicity, but Sorbitol had no adverse effects on the reproduction of CD rats during a multigeneration feeding study and was not a reproductive toxin at doses of 3000 to 7000 mg/kg/day for 2 years. Overall these esters and their corresponding fatty acids were not mutagenic, but Sorbitan Oleate was reported to reduce DNA repair following ultraviolet radiation exposure in human lymphocytes in culture. Sorbitan Laurate and Sorbitan Trioleate were cocarcinogens in one mouse study, but Sorbitan Trioleate and Sorbitan Oleate were not tumor promoters in another study. In clinical tests, Sorbitan fatty acid esters were generally minimal to mild skin irritants and were nonsensitizing, but Sorbitan Sesquioleate did produce an allergic reaction in fewer than 1% of patients with suspected contact dermatitis and addition of Sorbitan Sesquioleate to the components of a fragrance mix used in patch testing increased both irritant and allergic reactions to the fragrance mix. Careful consideration was made of the data on the cocarcinogenesis of Sorbitan Laurate and Sorbitan Trioleate, but the high exposure levels, high frequency of exposure, and absence of a dose-response led to the conclusion that there was not a cocarcinogenesis risk with the use of these ingredients in cosmetic formulations. Accordingly, these ingredients were considered safe for use in cosmetic formulat...

show abstract

Section: Genotoxicitymentioning

confidence: 99%

Final Report on the Safety Assessment of Sorbitan Caprylate, Sorbitan Cocoate, Sorbitan Diisostearate, Sorbitan Dioleate, Sorbitan Distearate, Sorbitan Isostearate, Sorbitan Olivate, Sorbitan Sesquiisostearate, Sorbitan Sesquistearate, and Sorbitan Triisostearate

Lanigan¹,

Yamarik²

2002

Int J Toxicol

View full text Add to dashboard Cite

show abstract

“…Contrary to our expectation, the PK activity in the livers of rats fed PB and a number of other hepatocarcinogenesis promoters was significantly and consistently lower than those fed the basal diet (12). The results led us to investigate the utility of the hepatic PK assay as a potential screening test for hepatocarcinogenesis promoter (13). In this review, we summarize our findings and discuss the strength and weakness of this assay.…”

Section: Introductionmentioning

confidence: 95%

Liver pyruvate kinase assay as a predicting screening test for promoters of hepatocarcinogenesis in the rat

Yanagi

1994

Journal of Environmental Science and Health, Part C

View full text Add to dashboard Cite

Effect of ethanol on hepatocarcinogenesis initiated in rats with 3′‐methyl‐4‐dimethylaminoazobenzene in the absence of liver injuries

Yanagi

Yamashita

Hiasa

et al. 1989

Intl Journal of Cancer

Self Cite

View full text Add to dashboard Cite

In this study special care was taken to discriminate between the direct effect of ethanol on hepatocarcinogenesis and secondary effects such as choline deficiency or fatty liver. Rats were divided into 2 groups, D and N. Group D was initiated using 3'-Me-DAB, while the control group N was not initiated. Groups N and D were divided into 4 sub-groups. Each subgroup was given, in the drinking water, one of the following ethanol solutions: 0, 5, 10 or 15% for 45 weeks. Liver tumors were induced only in D groups. Evidence obtained indicates that: (a) in the N group, ethanol did not cause any apparent disorders in histology and lipid metabolism, and (b) in the D group no significant differences were observed in the incidence of HCCs and other liver lesions. Ethanol thus does not appear to enhance hepatocarcinogenesis, at least in the absence of liver injury.

show abstract

Comparative study on pyruvate kinase activity‐reducing action of various promoters of hepatocarcinogenesis

Cited by 7 publications

References 12 publications

Final Report on the Safety Assessment of Sorbitan Caprylate, Sorbitan Cocoate, Sorbitan Diisostearate, Sorbitan Dioleate, Sorbitan Distearate, Sorbitan Isostearate, Sorbitan Olivate, Sorbitan Sesquiisostearate, Sorbitan Sesquistearate, and Sorbitan Triisostearate

Final Report on the Safety Assessment of Sorbitan Caprylate, Sorbitan Cocoate, Sorbitan Diisostearate, Sorbitan Dioleate, Sorbitan Distearate, Sorbitan Isostearate, Sorbitan Olivate, Sorbitan Sesquiisostearate, Sorbitan Sesquistearate, and Sorbitan Triisostearate

Liver pyruvate kinase assay as a predicting screening test for promoters of hepatocarcinogenesis in the rat

Effect of ethanol on hepatocarcinogenesis initiated in rats with 3′‐methyl‐4‐dimethylaminoazobenzene in the absence of liver injuries

Contact Info

Product

Resources

About