|1.||Roberts, R A: 3 articles (12/2000 - 02/2000)|
|2.||Hasmall, S C: 2 articles (12/2000 - 02/2000)|
|3.||Rabes, H M: 1 article (08/2001)|
|4.||Lamer, S: 1 article (08/2001)|
|5.||Klugbauer, S: 1 article (08/2001)|
|6.||Jungblut, P R: 1 article (08/2001)|
|7.||Dimitrijevic, N: 1 article (08/2001)|
|8.||Zeindl-Eberhart, E: 1 article (08/2001)|
|9.||West, D A: 1 article (12/2000)|
|10.||Olsen, K: 1 article (12/2000)|
08/01/1976 - "Given for 14 days, nafenopin reduced paralysis time to the same extent in both sexes. "
08/01/1976 - "In females, 3 days of nafenopin administration elicited a significant reduction of zoxazolamine paralysis time and an enhancement of its metabolism by the 9,000 g supernatant fraction of the liver. "
05/01/1993 - "The peroxisome proliferator (PP) nafenopin (NAF) enhanced tumor development in rat liver through promotion of a subtype of putative preneoplastic cell foci, characterized by weak cytoplasmic basophilia. "
06/15/1990 - "Tumor promotion by the peroxisome proliferator nafenopin involving a specific subtype of altered foci in rat liver."
01/01/1989 - "We will present evidence which strongly suggests that the peroxisome inducer, nafenopin (Naf), promotes tumor development in rat livers by stimulating selective growth of a hitherto undescribed subtype of altered foci. "
06/29/1995 - "Further studies are required to assess if the hepatocytes selected for clonal expansion by this EGF/nafenopin regime reflect the presumed pre-neoplastic cells induced by genotoxin in vivo and associated with an increased propensity to cancer."
07/11/1997 - "The effect of nafenopin-induced changes in the liver of rats on the toxicity of an anti-cancer drug cyclophosphamide was studied using cyto- and geno-toxicity parameters in the liver and bone marrow cells. "
06/01/1993 - "On the contrary, the hyperplasia induced by cyproterone acetate and nafenopin, which is characterized by a lack of increase in the expression of c-fos and c-jun, was also not associated with an increased c-myc expression. "
06/01/1993 - "When hyperplasia was induced by cyproterone acetate and nafenopin, the mitogenic response of the liver was not associated with an increased expression of c-jun or c-fos, despite the fact that the timing of the cell cycle was similar to that observed after partial hepatectomy. "
09/01/1998 - "Hyperplastic liver growth and regression of the hyperplasia were induced by treatment with cyproterone acetate (CPA) or nafenopin (NAF) followed by withdrawal; neither mRNAs of TGF-beta1 and TbetaR types I to III nor TGF-beta1 protein exhibited significant changes during the growth phase or during regression by apoptosis. "
05/01/1995 - "During involution of liver hyperplasia, which follows stopping treatment with the hepatomitogens cyproterone acetate (CPA) or nafenopin (NAF), numerous apoptotic hepatocytes could be observed with TUNEL-positive chromatin residues. "
05/01/1993 - "The inability of direct hyperplasia to stimulate the development of enzyme-altered hepatic foci was not unique to lead nitrate since the same phenomenon was observed when three other hepatomitogens, nafenopin, cyproterone acetate, and ethylene dibromide, were used."
04/15/1977 - "The nafenopin induced hepatomegaly therefore appears to arise from a combination of cell proliferation, as well as, cellular hypertrophy, which is associated with peroxisome proliferation."
09/01/1972 - "Studies on the hepatomegaly caused by the hypolipidemic drugs nafenopin and clofibrate."
09/01/1991 - "Nafenopin, LY171883 and clofibric acid were without effect on DNA replication on days 28-30 even though the hepatomegaly and induction of peroxisomal beta-oxidation persisted. "
02/01/1978 - "Treatment with all four drugs (clofibrate; its structural analogue, nafenopin; and two drugs structurally unrelated to clofibrate, tibric acid and Wy-14,643) produced a marked hepatomegaly in the mice. "
|5.||Body Weight (Weight, Body)
02/01/1991 - "Both food restriction and nafenopin treatment decreased body weight gain, but a decrease (14%) in fat content was only observed in nafenopin-treated rats. "
01/01/1997 - "In the present short term-study, we attempted to stimulate lipid peroxidation in male Wistar rats by (1) inducing PBOX enzymes with the peroxisome proliferator nafenopin at 90 mg/kg body weight per day in the diet for 10-11 days, and (2) by supplying the induced PBOX with an abundant amount of fatty acid as substrate, using a corn oil gavage at 20 ml/kg body weight. "
10/01/1996 - "Hepatocytes were isolated from nafenopin-treated animals (80 mg/kg body weight in 1.2 ml/kg body weight olive oil for 2 consecutive days) and exposed to various doses of 1,2 dichloroethane (DCE) (64-159 mumol) and 1,2-dibromoethane (DBE) (5.5-27.5 mumol) for up to 3 hr to assess the effect of nafenopin on the toxicity of dihaloalkanes. "
03/30/1988 - "Liver-weight to body-weight ratio, liver catalase, liver acyl-CoA oxidase, liver cell cytoplasmic eosinophilia, nuclear and cellular size, and peroxisomal staining were increased by the tumorigenic dose of lactofen, i.e., 250 ppm, in a fashion similar to the comparison chemical nafenopin (500 ppm), which is a peroxisome proliferator. "
|3.||Ethylene Dibromide (1,2 Dibromoethane)
|7.||Epidermal Growth Factor (EGF)
|8.||Hypolipidemic Agents (Antihyperlipidemics)
|10.||Corn Oil (Oil, Corn)