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PubMed1981

Novel multialveolar epithelial structures from rabbit mammary gland that synthesize milk specific fatty acids in response to prolactin.

Multialveolar mammary epithelial structures have been prepared from rabbit mammary gland by treating the tissue with collagenase plus hyaluronidase. These structures synthesize milk specific fatty acids when cultured with physiological concentrations (0.5 micrograms/ml) of prolactin in the presence of insulin and corticosterone. They have many of the advantages but few of the disadvantages of either mammary explants or primary cells in culture. For example, they are easily prepared in large numbers and respond to prolactin in culture even in the absence of serum or other tissue extracts. Because their level of organization is intermediate between that of explants and single cells, they provide a complementary system for studies on mammary differentiation.

Animals↗
PubMed1998

Tocotrienols inhibit the growth of human breast cancer cells irrespective of estrogen receptor status.

Potential antiproliferative effects of tocotrienols, the major vitamin E component in palm oil, were investigated on the growth of both estrogen-responsive (ER+) MCF7 human breast cancer cells and estrogen-unresponsive (ER-) MDA-MB-231 human breast cancer cells, and effects were compared with those of alpha-tocopherol (alphaT). The tocotrienol-rich fraction (TRF) of palm oil inhibited growth of MCF7 cells in both the presence and absence of estradiol with a nonlinear dose-response but such that complete suppression of growth was achieved at 8 microg/mL. MDA-MB-231 cells were also inhibited by TRF but with a linear dose-response such that 20 microg/mL TRF was needed for complete growth suppression. Separation of the TRF into individual tocotrienols revealed that all fractions could inhibit growth of both ER+ and ER- cells and of ER+ cells in both the presence and absence of estradiol. However, the gamma- and delta-fractions were the most inhibitory. Complete inhibition of MCF7 cell growth was achieved at 6 microg/mL of gamma-tocotrienol/delta-tocotrienol (gammaT3/deltaT3) in the absence of estradiol and 10 microg/mL of deltaT3 in the presence of estradiol, whereas complete suppression of MDA-MB-231 cell growth was not achieved even at concentrations of 10 microg/mL of deltaT3. By contrast to these inhibitory effects of tocotrienols, alphaT had no inhibitory effect on MCF7 cell growth in either the presence or the absence of estradiol, nor on MDA-MB-231 cell growth. These results confirm studies using other sublines of human breast cancer cells and demonstrate that tocotrienols can exert direct inhibitory effects on the growth of breast cancer cells. In searching for the mechanism of inhibition, studies of the effects of TRF on estrogen-regulated pS2 gene expression in MCF7 cells showed that tocotrienols do not act via an estrogen receptor-mediated pathway and must therefore act differently from estrogen antagonists. Furthermore, tocotrienols did not increase levels of growth-inhibitory insulin-like growth factor binding proteins (IGFBP) in MCF7 cells, implying also a different mechanism from that proposed for retinoic acid inhibition of estrogen-responsive breast cancer cell growth. Inhibition of the growth of breast cancer cells by tocotrienols could have important clinical implications not only because tocotrienols are able to inhibit the growth of both ER+ and ER- phenotypes but also because ER+ cells could be growth-inhibited in the presence as well as in the absence of estradiol. Future clinical applications of TRF could come from potential growth suppression of ER+ breast cancer cells otherwise resistant to growth inhibition by antiestrogens and retinoic acid.

Breast Neoplasms↗
PubMed1977

Immunological properties of medium-chain acyl-thioester hydrolase and fatty acid synthetase from lactating-rabbit mammary gland.

The cytosol from lactating-rabbit mammary gland contains a medium-chain acyl-thioester hydrolase. This hydrolase terminates chain lengthening of the fatty acids synthesised by fatty acid synthetase so as to release C8:0 and C10:0 fatty acids which are characteristic of rabbit milk. The medium-chain hydrolase and the fatty acid synthetase present in this cytosol have been shown to be immunologically distinct. When fatty acid synthetase was purified from this cytosol it showed unexpected immunological reactivity towards antiserum raised to the medium-chain hydrolase. The precipitate formed was not due to fatty acid synthetase, but to medium-chain hydrolase contaminating the synthetase. However, the proportion of this medium-chain hydrolase which was recovered with the purified synthetase was too small to be detected by sodium dodecyl sulphate-polyacrylamide gel electrophoresis, and was too small to elicit an antibody response in sheep. Immunological techniques have shown that the medium-chain hydrolase appears in rabbit mammary gland between days 17 and 22 of pregnancy. This coincides with the onset of milk-fat synthesis. The medium-chain hydrolase could not be detected in the cytosol from lactating-rabbit liver.

Animals↗
PubMed1990

Transport and cellular uptake of polychlorinated biphenyls (PCBs)--I. Association of individual PCB isomers and congeners with plasma lipoproteins and proteins in the pigeon.

Polychlorinated biphenyls (PCBs) are abundant and persistent pollutants in the ecosystem. Commercial mixtures (e.g. Aroclor 1254) can contain up to 80 different isomers and congeners, many of which accumulate in biological systems by the ingestion of PCB-contaminated lipid components of food chains. PCBs are lipophilic and lipid-rich lipoproteins provide an excellent system to transport PCBs to tissues. We report here the distribution of PCBs between plasma fractions in the pigeon. Twenty-four hours after injection, [14C]4-monochlorobiphenyl and [14C]2,2',5,5'-tetrachlorobiphenyl were associated with the protein-rich HDL fraction and the lipoprotein-poor fraction (predominantly albumin), rather than with the lipid-rich VLDL and LDL fractions. Five days after injection with the commercial PCB mixture Aroclor 1254, there was a distinctive distribution between the plasma fractions of the 41 congeners detected. Avian species have a poorly developed lymphatic system and dietary lipids are secreted into the portal vein. To emphasize this route of entry, the lipoprotein particles formed are termed portomicrons rather than chylomicrons. The most striking result was that the lipid-rich portomicron and the VLDL fraction was associated almost exclusively with only one congener (2,2',4,4'5,5'-hexachlorobiphenyl), whereas the other isomers and congeners were distributed amongst the LDL, HDL and the lipoprotein-poor (predominantly albumin) fractions. Thirteen of the congeners detected accounted for 74, 53 and 54%, respectively, of the total amount of PCBs in the LDL, HDL and lipoprotein-poor protein fractions. Five congeners that are highly toxic were enriched in the latter fraction. The distribution of PCBs is more complex than can be explained solely by their solubility in the lipid components of plasma fractions, and may suggest a complex association with apolipoproteins and plasma proteins that are important in transporting PCB to tissues. The identification of individual PCBs in lipoprotein fraction provides evidence for their role in the transport of lipophilic xenobiotics in blood and it is suggested that PCBs associated with lipoproteins are taken up by cells as lipoprotein-PCB complexes.

Animals↗
PubMed1990

Transport and cellular uptake of polychlorinated biphenyls (PCBs)--II. Changes in vivo in plasma lipoproteins and proteins of pigeons in response to PCBs, and a proposed model for the transport and cellular uptake of PCBs.

The complex distribution of polychlorinated biphenyl (PCB) isomers and congeners amongst plasma fractions of the pigeon suggests that the lipid and apolipoprotein components of lipoproteins, as well as plasma proteins, may be important in transporting PCBs to tissues (Borlakoglu et al., Biochem. Pharmac. 40, 265 (1990]. Pigeons were injected with the commercial PCB mixture Aroclor 1254 (1.5 mmol/kg body weight). After 120 hr triacylglycerol-like droplets accumulated in hepatocytes ('fatty liver syndrome'), there was proliferation of the hepatic smooth endoplasmic reticulum, and plasma concentrations of triacylglycerol and total cholesterol increased. This was accompanied by significant decreases in plasma concentrations of total protein, total apolipoproteins of the low density lipoprotein (LDL) and the high density lipoprotein (HDL) fractions, and albumin and by a significant increase in that of urea, indicating increased protein breakdown. These results suggest that Aroclor 1254 increased hepatic lipid synthesis, but decreased hepatic production of albumin and apolipoproteins. This would explain the accumulation of triacylglycerol in the liver and the increase in the proportion of triacylglycerol to apolipoprotein in the total lipoproteins. From the evidence presented, a model is proposed based on the association of PCBs with hydrophobic domains of lipids and proteins for the transport of PCBs by plasma fractions, their uptake into cells and intracellular metabolism, and their accumulation in adipose tissue.

Animals↗
PubMed1992

Lactational transfer of 3,3',4,4'-tetrachloro- and 2,2',4,4',5,5'-hexachlorobiphenyl induces cytochrome P450IVA1 in neonates. Evidence for a potential synergistic mechanism.

On the first day of lactation, material rats were treated with a single low dose of 5 mg/kg body weight of 3,3',4,4'-tetrachlorobiphenyl (TCB) or 2,2',4,4',5,5'-hexachlorobiphenyl (HCB) or with a combination of both congeners. Lactational transfer of these polychlorinated biphenyls (PCBs) was found in neonates and significant increases in microsomal cytochrome P450, cytochrome b5 and in glutathione-S-transferase activity were observed. Treatment with HCB did not increase neonatal ethoxyresorufin-O-de-ethylation (EROD) activities whereas a more than 26-fold increase in EROD activity was noted in response to exposure to TCB. However, EROD activities were increased more than 65-fold in response to the combined exposure to TCB and HCB. Exposure via milk to TCB caused a significant reduction in the N-demethylation of aminopyrine, but the combined exposure to TCB and HCB produced a significant reduction in the N-demethylation of dimethylnitrosamine. Lactational transfer of either TCB or HCB reduced marginally peroxisomal enzyme activities; however, exposure to a combination of TCB and HCB resulted in the highly significant reduction in KCN-insensitive palmitoyl-CoA oxidation and acetyl-CoA oxidation. Contrary to the reduction of these enzyme activities, the specific concentrations of CYP4A1 were significantly increased when neonates were exposed to either TCB or HCB. The largest induction, however, was observed in response to the combined exposure to both PCBs. Evidence is presented to suggest an induction of CYP4A1 which may be independent of the molecular substitution pattern of the two PCBs used in our studies but on a possible mode of synergistic interaction.

Animals↗
PubMed1989

Evidence for the induction of cytochrome P-452 in rat liver by Aroclor 1254, a commercial mixture of polychlorinated biphenyls.

We have examined the ability of a commercial mixture of polychlorinated biphenyls (Aroclor 1254) to induce hepatic cytochrome P-452-linked enzyme activities in rat and pigeon liver five days after its intraperitoneal injection. The results provide evidence that, at the doses used, Aroclor 1254 induces cytochrome P-452-linked enzyme activities in rats, but not in pigeons. This inductive effect was previously regarded as being specific for hypolipidemic drugs and phthalate ester plasticisers.

Animals↗