Detail of "33631-41-3"

Reference

Lack of inhibition by retinoids of bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian hamsters

Lack of inhibition by retinoids of bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian hamsters. Birt, Diane F.; Davies, Marc H.; Pour, Parviz M.; Salmasi, Shahrokh (Med. Cent., Univ. 4759-48-2 and 33631-48-0 are also occured in this study. Nebraska, Omaha, NE 68105, USA). Carcinogenesis (London), 4(10), 1215-20 (English) 1983. CODEN: CRNGDP. ISSN: 0143-3334. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Syrian hamsters were treated with either a low (10 mg/kg) or high (40 mg/kg) single dose of bis(2-oxopropyl)nitrosamine (BOP) [60599-38-4] and beginning 1 wk later fed either low (0.2 mmol/kg diet) or high (0.4-1.0 mmol/kg diet) levels of 1 of 4 retinoids [13-cis-retinoic acid (13-cis-RA) [4759-48-2], N-ethylretinamide (ERA) [33631-41-3], N-(2-hydroxyethyl)retinamide (OHERA) [33631-47-9], or N-(phenyl)retinamide (PRA) [33631-48-0]] for 40 or 50 wk. The high retinoid levels (0.4-1.0 mmol/kg diet) fed following the highest BOP treatment enhanced pancreatic carcinoma yields (av. no./effective animal) in males fed all 4 retinoids, and in females fed ERA and 13-cis-RA. Enhanced adenoma yields were also seen in all groups when high retinoid levels were fed following 40 mg BOP/kg. Similarly, tumor yields at extrapancreatic sites were elevated in retinoid-fed hamsters of both sexes after 40 mg BOP/kg. However, these retinoid levels caused an increased adenoma yield in male hamsters only and did not modify carcinoma yields when fed following 10 mg BOP/kg. Similarly, tumor yields at extrapancreatic sites were elevated in retinoid-fed hamsters of both sexes after 40 mg BOP/kg and in males fed ERA and 13-cis-RA after 10 mg BOP/kg when retinoids were given at the high levels (0.4-1.0 mmol/kg diet). Increased incidences of bile duct and liver tumors in particular were found in hamsters given 40 mg BOP/kg. Consumption of retinoid levels of 30.4 mmol/kg diet was also assocd. with a high incidence of liver cell necrosis, ovarian cysts, and ovarian hemorrhage. Retinoids (ERA, OHERA, and PRA) fed at the low level (0.2 mmol/kg diet) following the low BOP dose did not enhance carcinogenesis in the pancreas or at other sites and did not cause alterations in morphol. observations. .

Amelioration of embryotoxicity by structural modification of the terminal group of cancer chemopreventive retinoids

Amelioration of embryotoxicity by structural modification of the terminal group of cancer chemopreventive retinoids. Willhite, Calvin C.; Shealy, Y. Fulmer (Toxicol. Res. Unit, West. Reg. Res. Cent., Berkeley, CA 94710, USA). JNCI, J. Natl. Cancer Inst., 72(3), 689-95 (English) 1984. CODEN: JJIND8. ISSN: 0198-0157. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 18 An oral dose of all-trans-retinoic acid [302-79-4] or 13-cis-retinoic acid [4759-48-2] in the pregnant [Lak:LVG(SYR)] hamster caused a dose-dependent increase in malformations in the offspring, but an equiv. dose of all-trans-N-ethylretinamide (I) [33631-41-3] or 13-cis-N-ethylretinamide [75686-04-3] failed to result in embryotoxicity. 302-79-4 and 11103-57-4 which are cas registry numbers of substances are two of reagents here. Apparently, structural modification of the retinoid skeleton can produce compds. that retain cancer chemopreventive activity but that lack the teratogenic activity common to many synthetic and naturally occurring forms of vitamin A [11103-57-4]. Thus, in the retinoids, the 2 kinds of activity, interference with the process of carcinogenesis and interference with embryonic development, may be divorced. .