A trans-Atlantic examination of haddock Melanogrammus aeglefinus food habits.

The food habits of Melanogrammus aeglefinus were explored and contrasted across multiple north-eastern and north-western Atlantic Ocean ecosystems, using databases that span multiple decades. The results show that among all ecosystems, echinoderms are a consistent part of M. aeglefinus diet, but patterns emerge regarding where and when M. aeglefinus primarily eat fishes v. echinoderms. Melanogrammus aeglefinus does not regularly exhibit the increase in piscivory with ontogeny that other gadoids often show, and in several ecosystems there is a lower occurrence of piscivory. There is an apparent inverse relationship between the consumption of fishes and echinoderms in M. aeglefinus over time, where certain years show high levels of one prey item and low levels of the other. This apparent binary choice can be viewed as part of a gradient of prey options, contingent upon a suite of factors external to M. aeglefinus dynamics. The energetic consequences of this prey choice are discussed, noting that in some instances it may not be a choice at all.

[Cholesterol esterification in tissues and change in the apoprotein spectrum in rat blood under the effect of auto-oxidized cholesterol]. / Esterifikatsiia kholesterina v tkaniakh i izmenenie apoproteidnogo spektra v plazme krovi krys pri vozdeistvii avtookislennogo kholesterina.

Influence of autooxidized cholesterol (Ch) products on accumulation of cholesterol esters (ChE) in liver and aorta tissues as well as alteration of the apolipoprotein spectrum in low density and very low density (LDL and VLDL) lipoproteins in blood plasma was studied in rats treated with purified Ch (ChP-rats) and with oxidized Ch containing 5% 25-hydroxyCh and 3% 7-ketoCh (ChO-rats). Increase of ChE content in liver tissue of ChO-rats resulted in two-fold activation of acyl-CoA-cholesterol-O-acyltransferase (ACAT) in liver microsomes as compared with the enzymatic activity rate in ChP-rats. As shown by polyacrylamide gel electrophoresis content of apoE in VLDL and LDL of ChO-rats was 1,5-fold higher as compared with that of ChP-rats. Content of apoIV was increased in LDL and VLDL of ChP-rats as compared with controls; this effect was not observed in ChO-rats. LDL and VLDL from ChO-rats stimulated incorporation of 14C-oleate into ChE of cultivated macrophages. Increase in content of ChE found in aorta of ChO-rats appears to occur due to activation of Ch esterification. Intensification of ChE synthesis in tissues and alterations in the spectrum of LDL and VLDL apolipoproteins caused by oxidized products of cholesterol may be one of the mechanisms involved in atherogenesis.

[Effects of tocopherol on functional reserves of phagocytes]. / Vliianie tokoferola na funktsional'nye rezervy fagotsitov.

The addition of alpha-tocopherol into rats died (4 mg a day during 7 days) brings a twofold increase in tocopherol content in blood plasma and 1,3 fold increase in peritoneal macrophages. Viscosity of membrane lipids of macrophages was decreased. Control and experimental macrophages had identical activity of oxygen-dependent processes and ability for cholesterol esterification.

[Esterification of cholesterol oxidation products and their effect on the rate of cholesterol esterification in macrophages]. / Esterifikatsiia okislennykh produktov kholesterina i ikh vliianie na skorost' ésterifikatsii kholesterina v makrofagakh.

Effects of cholesterol (CH) autooxidation products on incorporation of 14C-oleate into cholesteryl esters (CE) and their possible esterification were studied in cultivated mice peritoneal macrophages (MPM). 25 Mg/ml of purified CH and 25 Mg/ml of autooxidized CH stimulated (4- and 17-fold, respectively) the cholesterol esterification in MPM. In presence of 4 Mg/ml 25-hydroxy CH or the mixture of 4 Mg/ml 7 alpha-, 7 beta-hydroxy CH and 7-keto CH incorporation of oleate into cellular CE was increased 20- and 4-fold, respectively. 4 Mg/ml concentration of cholestane-3 beta, 5 alpha, 6 beta-friol caused no effects. Mono- and diesters of 14C-hydroxy CH were found after 8 hrs incubation of the steroid with MPM. Incorporation of 14C-25 hydroxy CH into its esters occurred at the rate, which exceeded 6-7-fold the 14C-CH incorporation into CE. Esterification of 7 alpha-, 7 beta-hydroxyCH and 7-ketoCH was studied, 0.52% label of the total cell sterols radioactivity was detected in the fraction of nonpolar steroids. 14C-cholestane-3 beta,5 alpha,6 beta-triol was not esterified in MPM. The stimulating effects of 25-hydroxyCH on oleate incorporation into CE and its esterification in MPM were inhibited in presence of 10 Mg/ml progesterone, an inhibitor of acyl-CoA:cholesterol acyltransferase activity. Induction of CE formation in MPM by means of choltransferase activity. Induction of CE formation in MPM by means of cholesterol oxidation products may be responsible for development of foam cells, while esterification of polar steroids in cells appears to be of importance in decrease of their toxic and metabolic effects.

[Effect of the monooxygenase activity inhibitor ketoconazole on cholesterol esterification in mouse peritoneal macrophages]. / Vliianie ingibitora monooksigenaznoi aktivnosti ketokonazola na ésterifizkatsiiu kholesterina v peritoneal'nykh makrofagakh myshi.

In order to determine the feasible role of monooxygenases in regulation of the macrophage acyl-CoA: cholesterol acyltransferase (ACAT) activity, the effects of ketoconazole on the activities of benz(a)pyrene hydroxylase and ACAT as well as on the [14C]oleate incorporation into cholesterol esters in cultured mouse peritoneal macrophages (MPM) were studied. Ketoconazole (0.5-50 M) inhibited the benz(a)pyrene hydroxylase activity but increased the free cholesterol (FC) level in MPM cultured with an acetylated low density lipoprotein (acetyl-LDL). An addition of ketoconazole (1-50 M) eliminated the increase in the rate of FC esterification after incubation of MPM with acetyl-LDL (but not with 25-hydroxycholesterol). In contrast, progesterone, an ACAT activity inhibitor, used at 5-30 M diminished the rate of FC esterification, when MPM were incubated with acetyl-LDL of 25-hydroxycholesterol. Ketoconazole provoked a dose-dependent decrease of the [3H]FC incorporation into macrophage polar oxysteroids. The data obtained suggest that the ketoconazole (1-30 M) effect on FC esterification in MPM cultured with acetyl-LDL is determined by its inhibiting monooxygenases, which produce oxidized forms of FC that are potential activators of ACAT.

[The effect of progesterone on metabolism of cholesterol esters in macrophages cultured with acetylated low density lipoproteins]. / Vliianie progesterona na metabolizm éfirov kholesterina v makrofagakh,kul'tiviruemykh s atsetilirovannymi lipoproteidami nizkoi plotnosti.

Effect of progesterone on esterification of free cholesterol, on content of free cholesterol and its esters was studied in rat macrophages, cultivated in presence of acetyl-derivatives of low density lipoproteins (Ac-LDL), as well as on mobilization of cholesterol from macrophages. Progesterone at a dose of 0.5-10 micrograms per I ml of cultivating medium caused dose-dependent inhibition of I-14C-oleate incorporation into cholesterol esters of macrophages cultivated with Ac-LDL (50 micrograms of protein/ml). In the medium free of LDL progesterone caused an increase of cholesterol in macrophages by 45%, while addition of 100 micrograms/ml LDL led to a decrease of free cholesterol by 20% of the initial level. If macrophages pre-enriched with 4-C14-cholesterol were cultivated in LDL containing medium, progesterone increased the 4-14C-cholesterol liberation into medium and decreased the cholesterol content in macrophages. Under conditions of macrophages incubation in the LDL-free medium, progesterone increased the free cholesterol content in these cells but did not affect the 4-14C-cholesterol liberation into medium. The data obtained suggest that the progesterone-induced inhibition of free cholesterol esterification may increase its mobilization from macrophages only if the LDL acceptor function is unaltered.

[The effect of dibutyryl cAMP, verapamil and adrenaline on cholesterol mobilization from macrophages]. / Vliianie dibutiril-tsAMF, verapamila i adrenalina na mobilizatsiiu kholesterina iz makrofagov.

The capacity of dibutyryladenosine-3':5'-cyclic phosphate (dibutyryl cAMP), verapamil and epinephrine to modulate cholesterol (CH) excretion was studied in the stored (4-14C)-CH rat macrophages. The experiments indicated that in the absence of high density lipoproteins (HDL) the addition of dibutyryl cAMP (0.2 mmol), verapamil (0.05 mmol), epinephrine (0.05 mmol) in cultured medium did not influence the excretion of the stored (4-14C)-CH from macrophages during 4, 8 and 18 hours. The addition of the drugs in the presence of HDL resulted in an increase in the excretion of (4-14C)-CH from macrophages during incubation. The data indicate that the drugs which increase the cellular concentration of cAMP can induce the mobilization of CH from macrophages in the presence of acceptors of CH.

[Skin cholesterol level and its correlation with the lipid indicators of the blood serum in healthy persons and in patients with ischemic heart disease]. / Soderzhanie kholesterina v kozhe i ego korreliatsiia s lipidnymi pokazateliami syvorotki krovi u zdorovykh liudei i bol'nykh ishemicheskoi bolezn'iu serdtsa.

Skin free and esterified cholesterol in the forearm and serum lipid levels were examined in 42 male coronary patients and 46 normal male subjects. Irrespective of the type of dislipoproteinemia or normolipidemia, total cholesterol and its free fraction appear to be significantly increased in coronary patients, as compared to normal subjects. There were no significant correlations between the examined skin and serum parameters, either in coronary patients, or in the controls. Possible use of skin cholesterol measurement in the diagnosis of lipid disturbances leading to atherosclerosis is discussed.

[Lecithin-cholesterol-acyltransferase activity in chronic liver diseases]. / Aktivnost' letsitin-kholesterol-atsiltransferasy pri khronicheskikh zabolevaniiakh pecheni.

Activity of lecithin-cholesterol-acyl transferase (LCAT) was distinctly decreased in chronic impairments of liver tissue, especially under conditions of liver cirrhosis and hepatocellular cancer. After treatment with "essentiale forte" the enzymatic activity was elevated only in the patients with chronic hepatitis. The LCAT activity correlated with content of albumins, gamma-globulins and the data of thymol test. Estimation of the LCAT activity might serve as a diagnostic test in chronic liver tissue diseases.

[Cholesterol esterase activity in the rat aorta and liver after stimulation and blockade of beta-adrenergic receptors]. / Aktivnost' kholesterolésteraz v aorte i pecheni krysy pri stimuliatsii i blokade beta-adrenoretseptorov.

Activities of lysosomal and cytoplasmic cholesterol esterases and cholesterol content in rat blood serum, liver tissue and aorta were studied after administration of ephedrine and propranolol. The ephedrine-induced lipolytic effect was fully inhibited by propranolol. The correlation between stimulation of beta-adrenergic receptors and activation of lipolytic enzymes was found.

[Prevention of damages to the microsomal monooxygenases in thermal ischemia of the liver by the separate and combined use of alpha-tocopherol, lidocaine and kontrikal]. / Profilaktika povrezhdenii mikrosomal'nykh monooksigenaz pri teplovoi ishemii pecheni razdel'nym i kombinirovannym primeneniem al'fa-tokoferola, lidokaina i kontrikala.

It was found in experiments on the in vitro model of rat liver ischemia that ischemia initiates membrane lipid peroxidation and proteolysis leading to damage of monooxygenase enzyme systems of microsomes. Preventive administration of alpha-tocopherol, lidocaine, contrykal and their combinations revealed the optimal protective effect of the combined administration of alpha-tocopherol with lidocaine and alpha-tocopherol with contrykal as compared to their separate use on the functional activity of microsomal monooxygenases at thermal ischemia of the liver. A combined approach to prevention of impairment of the liver function at its ischemia was recommended.

[Effect of 17 alpha-ethinyl estradiol on the blood serum lipid indices of rats]. / Vliianie 17 al'fa-étiniléstradiola na lipidnye pokazateli syvorotki krovi krys.

The administration of 17-ethinyl estradiol (0.25 mg/kg) to male Wistar rats caused on the 3rd day a decrease of the levels of free and esterified cholesterol, blood serum triglycerides and also a reduction of the content of esterified cholesterol with respect to total cholesterol while the lecithin-cholesterol-acyltransferase activity appeared to be unchanged. The effect of ethinyl estradiol on blood lipid parameters against the background of lipemia induced by triton WR 1339 was reduced.

[Changes in the activity of enzymes of cholesterol esters synthesis and hydrolysis in rat adrenals after treatment with 17 alpha-ethinyl estradiol]. / Izmenenie aktivnosti fermentov sinteza i gidroliza éfirov kholesterina v nadpochechnikakh krysy pri vozdeistvii 17 alpha-étiniléstradiola.

A study was made of the effect of hypocholesterolemia induced by 3-day administration of 17 alpha-ethinyl estradiol on the activity of lysosomal and cytoplasmatic cholesterol esterases, acyl-CoA: cholesterol acyltransferase and on the free and esterified cholesterol concentrations in the rat adrenals. A decrease in the content of esterified cholesterol in the adrenal tissue was accompanied by a decrease in the activity of acyl-CoA: cholesterol acyltransferase and by an increase in the activity of lysosomal cholesterol esterase. The activity of cytoplasmatic cholesterol esterase was not changed significantly. The data obtained were discussed with relation to the synthesis of steroid hormones in the rat adrenals.

[Effect of 17 alpha-ethinylestradiol on the activity of enzymes synthesizing and hydrolyzing cholesterol esters in the rat liver]. / Vliianie 17 al'fa-étiniléstradiola na aktivnost' fermentov sinteza igidroliza éfirov kholesterina v pecheni krysy.

Intraperitoneal injection of 25 micrograms/100 g body weight of 17 alpha-ethinyl estradiol to rats was shown to decrease serum cholesterol and to increase hepatic cholesterol. The rise in the level of non-labeled and C14-labeled free and esterified cholesterol in hepatic homogenate, as well as in lysosomal and cytosol fractions was accompanied by reduced activity of acyl-CoA-cholesterol acyltransferase and increased activity of lysosomal cholesterol esterase, as compared with the controls. The activity of cytoplasmic cholesterol esterase remained practically unchanged. Fistula bile of treated rats collected during 30 min was analyzed for the concentration of free cholesterol and bile acids. It has been shown that treatment of rats with 17 alpha-ethinyl estradiol caused an increase in hepatic cholesterol elimination via bile pathways.

[Activity of key enzymes of cholesterol biotransformation and lipid content in the liver, aorta, adrenals and blood of rats exposed to chloroquine]. / Aktivnost' kliuchevykh fermentov biotransformatsii kholesterina i soderzhanie lipidov v pecheni, aorte, nadpochechnikakh i krovi krys pri vozdeistvii khlorokhina.

Intraperitoneal administration of chloroquine (50 mg/kg, 7 days) to rats was followed by the increase of cholesterol, its esters, triglycerides and phospholipids levels in tissues, the decrease of lysosomal cholesterol esterase and acyl-koA-cholesterol acyl transferase activity in the liver and the enhancement of the non-sedimentable activity of acid phosphatase and beta-galactosidase. At concentration range of 3.5 to 140 mM the drug inhibited the activity of cholesterol esterase in the rat liver lysosome fraction.

[Activity of cholesterol metabolism enzymes and lipid levels in the rat liver, aorta, adrenals and serum after exposure to triton WR 1339]. / Aktivnost' fermentov kholesterinovogo metabolizma i soderzhanie lipidov v pecheni, aorte, nadpochechnikakh i syvorotke krovi krysy pri vozdeistvii tritona WR 1339.

Injection of Triton WR 1339 into Wistar rats caused a marked increase in contents of free and ester-bound cholesterol, triglycerides, phospholipids and free fatty acids in tissues and a decrease in the activity of lecithin: cholesterol acyltransferase in blood. An increase in concentration of cholesterol esters in tissues was due to a decrease in activity of lysosomal cholesteryl esterase in vivo and in vitro and to an increase in non-sedimentable activities of acid phosphatase, beta-galactosidase and cholesteryl esterase. The decrease in proteolytic degradation of cholesterol esters was accompanied by an increase in the activity of tissue cytoplasmic cholesteryl esterase and by a decrease in activity of acyl-CoA: cholesterol O-acyltransferase in liver tissue.

[Mechanisms of the damage to the liver monooxygenase systems in thermal ischemia]. / Mekhanizmy povrezhdeniia monooksigenaznykh sistem pecheni pri teplovoi ishemii.

It was shown in experiments in vitro that thermal ischemia of liver tissue leads to disorders in the function of membrane-bound microsomal monooxygenases. Disorders in the structural organization of membranes were also expressed in the inhibition of reactions of ascorbate-depending and fermentative peroxide oxidation of lipids and labilization of lysosomal membranes. Faults in the rate of amidopyrine n-demethylation and aniline n-hydroxylation correlate with the intensification of spontaneous peroxidation of lipids and activation of proteolytic processes in ischemia. The obtained data permitted to ground the approach to pharmacological prophylaxis of ischemic damages of liver microsomal monooxygenases.

[Structural-functional aspects of the postischemic recovery of the hepatocyte endoplasmic network in rats]. / Strukturno-funktsional'nye aspekty postishemicheskogo vosstanovleniia éndoplazmaticheskoi seti gepatotsitov krys.

The experiments on rats have shown that total hepatic ischemia reduces the content of microsomal cytochromes P-450 and b5 and causes amidopyrine and aniline disturbances over a 2-3-week post-ischemic period. The analysis of hepatocyte ultrastructure has revealed the interdependence of structural and functional changes in endoplasmic reticulum during recovery period. The damage of monooxygenase inducibility correlated with stable decline in the number of fixed ribosomes in post-ischemic period.