Bio-availability and metabolism of n-3 fatty acid rich garden cress (Lepidium sativum) seed oil in albino rats

The ratio of fatty acids namely linoleic acid (LA, 18:2, n-6) and alpha linolenic acid (ALA, 18:3, n-3) in the diet plays an important role in enrichment of ALA in tissues and further conversion to long-chain polyunsaturated fatty acids (LC-PUFA) like eicosapentaenoic acid (EPA, 20:5, n-3) and docosahexaenoic acid (DHA, 22:6, n-3). Garden cress seed oil (GCO) is one of the richest sources of omega-3 fatty acid and contains 29-34.5% of ALA. In this study, dietary supplementation of GCO on bio-availability and metabolism of alpha-linolenic acid was investigated in growing rats. Male wistar rats were fed with semi-purified diets supplemented with 10.0% sunflower oil (SFO 10%); 2.5% GCO and 7.5% SFO (GCO 2.5%); 5% GCO and 5% SFO (GCO 5.0%); 10% GCO (GCO 10%) for a period of 8 weeks. There was no significant difference with regard to the food intake, body weight gain and organ weights of rats in different dietary groups. Rats fed with GCO showed significant increase in ALA levels in serum and tissues compared to SFO fed rats. Feeding rats with 10% GCO lowered hepatic cholesterol by 12.3% and serum triglycerides by 40.4% compared to SFO fed group. Very low density lipoprotein cholesterol (VLDL-C) and low density lipoprotein cholesterol (LDL-C) levels decreased by 9.45% in serum of 10% GCO fed rats, while HDL remained unchanged among GCO fed rats. Adipose tissue showed incorporation of 3.3-17.4% of ALA and correlated with incremental intake of ALA. Except in adipose tissue, the EPA, DHA levels increased significantly in serum, liver, heart and brain tissues in GCO fed rats. A maximum level of DHA was registered in brain (11.6%) and to lesser extent in serum and liver tissues. A significant decrease in LA and its metabolite arachidonic acid (AA) was observed in serum and liver tissue of rats fed on GCO. Significant improvement in n-6/n-3 fatty acid ratio was observed in GCO based diets compared to diet containing SFO. This is the first study to demonstrate that supplementation of GCO increases serum and liver ALA, EPA, DHA and decreases LA and AA in rats. Therefore, the GCO can be considered as a potential, alternate dietary source of ALA.     

Tissue blood flow in control and cold-adapted hyperthyroid rats

Chronic injections (once daily for 10-14 days) of triiodothyronine (T3) stimulated oxygen consumption by 50 and 15% in anaesthetized, control (24 degrees C), and cold-adapted (5 degrees C) rats, respectively, compared with euthyroid controls. Tissue blood flow, determined from the distribution of radioactive microspheres, was unaffected by T3 treatment in skeletal muscle, scrotum, brain, bone, skin, diaphragm, and brown adipose tissue (BAT) of rats housed at 24 degrees C, but was decreased in spleen (53% of control) and significantly increased in three white adipose tissue depots (average 267% increase) and liver (56%). Blood flow to epididymal fat and leg muscle of cold-adapted rats was increased by T3 treatment (100 and 138% increases, respectively), but other tissues were unaffected. Blood oxygen extraction and oxygen consumption in vivo by interscapular BAT was increased in hyperthyroid rats compared with euthyroid controls, but was reduced by T3 treatment in cold-adapted animals. These data show that BAT makes only a minor contribution (7%) to thyroid thermogenesis, but suggest that kidney, liver, gut, and particularly white adipose tissue may be involved.     

Isomers of conjugated linoleic acid decrease plasma lipids and stimulate adipose tissue lipogenesis without changing adipose weight in post-prandial adult sedentary or trained Wistar rat

The respective effects and interactions of supplementation with two conjugated linoleic acid (CLA) isomers and exercise on plasma metabolic profile, activity of lipogenic enzymes and cellularity in two adipose tissue sites, those of the liver and heart, were examined in adult Wistar rats. Rats that were either sedentary or exercise-trained by treadmill running were fed one of four diets: a diet without CLA; a diet with either 1% cis 9, trans 11 CLA or 1% trans 10, cis 12 CLA; or a mixture of both isomers (1% of each) for 6 weeks. We observed that the exercise decreased lipogenic enzyme activities in epididymal and perirenal adipose tissue. Plasma cholesterol, insulin, and leptin concentrations were lower in exercise-trained rats than in sedentary rats. The ingestion of either CLA mixture or the trans 10, cis 12 CLA increased lipogenic enzyme activities in epididymal tissue and more markedly in perirenal adipose tissue, especially in sedentary rats, and without affecting adipose tissue weight or cellularity. A similar effect of trans 10, cis 12 CLA was observed in regard to malic enzyme activity in the liver. In addition, this isomer decreased plasma lipid and urea concentrations and increased plasma 3-hydroxybutyrate levels. The ingestion of cis 9, trans 11 CLA increased fatty acid synthase activity in perirenal adipose tissue in sedentary rats and decreased plasma cholesterol and leptin concentrations. These results show that isomers of CLA decrease plasma lipids and stimulate adipose tissue lipogenesis without changing adipose weight in adult sedentary or exercise-trained rat, thus suggesting a stimulation of adipose tissue turnover.     

3H]thymidine incorporation into whole liver as an alternative to [3H]thymidine incorporation into DNA as a parameter of cell proliferation in regenerating liver tissue in rats

OBJECTIVE: To monitor liver regeneration following partial hepatectomy, liver cell proliferation can be measured by assaying in vivo [3H]thymidine incorporation into liver cell DNA. We hypothesized that [3H]thymidine incorporation into whole liver tissue parallels [3H]thymidine incorporation into liver cell DNA, both in high proliferating and low proliferating liver. STUDY DESIGN: Liver cell proliferation in rats after partial hepatectomy or a sham operation was studied by measuring incorporation of [3H]thymidine into various fractions of liver tissue on days 1, 2, 3, 4 and 10 after surgery. RESULTS: [3H]thymidine incorporation into whole liver tissue and in the protein fraction correlated well with DNA-specific [3H]thymidine incorporation into regenerating (r > .80, P < .0001) and nonregenerating liver (r > .69, P < .005). [3H]thymidine incorporation into DNA was < 5% of the total amount of administered [3H]thymidine in both sham-operated and hepatectomized rats. Significant differences in [3H]thymidine incorporation into partially hepatectomized livers as compared to sham-operated rat livers were found on days 1 and 2 (whole liver tissue and protein fraction) or day 1 (DNA) after surgery. CONCLUSION: [3H]thymidine incorporation into whole liver tissue is a simple technique that can be used for the study of liver cell proliferation after partial hepatectomy in rats.     

Effects of glucose-containing peritoneal-dialysis solutions on rates of lipogenesis in vivo in the liver, brown and white adipose tissue of chronic uraemic rats.

Chronic uraemic rats had decreased food intake, and this was accompanied by decreased weight of the epididymal fat-pads and interscapular brown adipose tissue. Normal rats whose food intake was restricted to an amount similar to that of the uraemic rats showed similar decreases in weight of the adipose-tissue depots. In addition, the food-restricted rats had decreased liver weight compared with normal or uraemic rats. The basal rate of lipogenesis was decreased in liver and epididymal fat-pads of food-restricted and uraemic rats and in interscapular brown adipose tissue of uraemic rats. Administration of a low-glucose-containing (1.36%) peritoneal-dialysis solution slightly increased lipogenesis in liver of uraemic rats, but had no significant effect in epididymal fat-pads. For brown fat, the rate of lipogenesis was increased in normal, food-restricted and uraemic groups, but the values for the last group were 4-5-fold lower than for the food-restricted or control groups. A high-glucose-containing (3.86%) peritoneal-dialysis solution gave similar rates of lipogenesis in liver, epididymal fat-pads and brown fat of all three groups, but for brown fat moderately uraemic rats showed a considerably lower rate of lipogenesis than did mildly uraemic rats. The basal plasma insulin concentration was lower in the food-restricted (50%) and uraemic (70%) groups than in the control group. The low-glucose peritoneal-dialysis solution increased plasma insulin to control values in the food-restricted rats, but had no significant effect on plasma insulin in the uraemic rats, despite a significant increase in blood glucose in this group. It is concluded that there is an impairment of the lipogenic response to intraperitoneal glucose loads in interscapular brown adipose tissue of uraemic rats, and that this is not due to the accompanying decrease in food intake. The hypoinsulinaemia may be an important factor. The possible relevance of this finding to the obesity observed in some uraemic patients treated by peritoneal dialysis with glucose-containing solutions is discussed.     

Adipose tissue compensates for defect of phosphatidylinositol 3'-kinase induced in liver and muscle by dietary fish oil in fed rats

The present work aimed to study in rats whether substitution of a low level of fish oil (FO; 2.2% of calories) into a low-fat diet (6.6% of calories from fat as peanut-rape oil or control diet) 1) has a tissue-specific effect on insulin signaling pathway and 2) prevents dexamethasone-induced alteration of insulin signaling in liver, muscle, and adipose tissue. Sixteen rats were used for study of insulin signaling, and sixteen rats received an oral glucose load (3 g/kg). Eight rats/group consumed control diet or diet containing FO over 5 wk. Four rats from each group received a daily intraperitoneal injection of saline or dexamethasone (1 mg.kg(-1).day(-1)) for the last 5 days of feeding. In liver, FO decreased phosphatidylinositol 3'-kinase (PI 3'-kinase) activity by 54% compared with control diet. A similar result was obtained in muscle. In both liver and muscle, FO clearly amplified the effect of dexamethasone. FO did not alter early steps of insulin signaling, and in muscle GLUT4 protein content remained unaltered. In adipose tissue, FO increased PI 3'-kinase activity by 74%, whereas dexamethasone decreased it by 65%; inhibition of PI 3'-kinase activity by dexamethasone was similar in rats fed FO or control diet, and GLUT4 protein content was increased by 61% by FO. Glycemic and insulinemic responses to oral glucose were not modified by FO. In conclusion, FO increased PI 3'-kinase activity in adipose tissue while inhibiting it in liver and muscle. The maintenance of whole body glucose homeostasis suggests an important role of adipose tissue for control of glucose homeostasis.     

Augmented efficacy of tamoxifen in rat breast tumorigenesis when gavaged along with riboflavin, niacin, and CoQ10: effects on lipid peroxidation and antioxidants in mitochondria

Reactive oxygen species (ROS) play a major role in causing mitochondrial changes linked to cancer and metastasis. Uptake of antioxidants by tissue to reduce the ROS production could be instrumental in controlling cancer. Tamoxifen (TAM), a nonsteroidal anti-estrogen drug most used in the chemotherapy and chemoprevention of breast cancer. Riboflavin, niacin and coenzyme Q10 (CoQ10) are proved to be potent antioxidants and protective agents against many diseases including cancer. The objective of this research is to determine the therapeutic efficacy of combinatorial therapy on mammary carcinoma bearing rats in terms of the mitochondrial lipid peroxidation and antioxidant status especially MnSOD. Female albino rats of Sprague-Dawley strain were selected for the investigation. Mammary carcinoma was induced with 7,12-dimethyl benz(a)anthracene (DMBA: 25 mg), and the treatment was started by the oral administration of TAM (10 mg/kg body weight/day) along with riboflavin (45 mg/kg body weight/day), niacin (100 mg/kg body weight/day) and CoQ10 (40 mg/kg body weight/day) for 28 days. The levels of lipid peroxides, activities of enzymic and non-enzymic antioxidants were measured in the mitochondria isolated from the mammary gland and liver of control and experimental rats. Rats treated with DMBA showed an increase in mitochondrial lipid peroxidation (mammary gland 52.3%; liver 25.1%) accompanied by high malondialdehyde levels along with lowered activities of mitochondrial enzymic antioxidants [superoxide dismutase (mammary gland 19.9%; liver 24.8%), catalase (mammary gland 50%; liver 19.7%), glutathione peroxidase (mammary gland 47.8%; liver 31.1%)] and non-enzymic antioxidants [reduced glutathione (mammary gland 14.3%; liver 13.3%), Vitamin C (mammary gland 6.49%; liver 21.4%) and E (mammary gland 20.3%; liver 22.2%)]. Administration of combinatorial therapy restored lipid peroxide level and the activities of enzymic and non-enzymic antioxidants to near normalcy. In addition, antitumour activity was also found to be enhanced which is evident from the increased expression of tumour suppressor gene MnSOD thereby preventing cancer cell proliferation. These results suggested that TAM treatment is the most effective during co-administration of riboflavin, niacin and CoQ10 in terms of mitochondrial antioxidant and antitumour activity.     

Cardiac,skeletal muscle and serum irisin responses to with or without water exercise in young and old male rats: Cardiac muscle produces more irisin than skeletal muscle

Irisin converts white adipose tissue (WAT) into brown adipose tissue (BAT), as regulated by energy expenditure. The relationship between irisin concentrations after exercise in rats compared humans after exercise remains controversial. We therefore: (1) measured irisin expression in cardiac and skeletal muscle, liver, kidney, peripheral nerve sheath and skin tissues, as also serum irisin level in 10 week-old rats without exercise, and (2) measured tissue supernatant irisin levels in cardiac and skeletal muscle, and in response to exercise in young and old rats to establishing which tissues produced most irisin. Young (12 months) and old rats (24 months) with or without 10 min exercise (water floating) and healthy 10 week-old Sprague-Dawley rats without exercise were used. Irisin was absent from sections of skeletal muscle of unexercised rats, the only part being stained being the perimysium. In contrast, cardiac muscle tissue, peripheral myelin sheath, liver, kidneys, and skin dermis and hypodermis were strongly immunoreactivity. No irisin was seen in skeletal muscle of unexercised young and old rats, but a slight amount was detected after exercise. Strong immunoreactivity occurred in cardiac muscle of young and old rats with or without exercise, notably in pericardial connective tissue. Serum irisin increased after exercise, being higher in younger than older rats. Irisin in tissue supernatants (cardiac and skeletal muscle) was high with or without exercise. High supernatant irisin could come from connective tissues around skeletal muscle, especially nerve sheaths located within it. Skeletal muscle is probably not a main irisin source.     

Heme oxygenase activity as measured by carbon monoxide production

A method is described for the in vitro determination of heme oxygenase (HO) activity in animal tissue preparations through determination of carbon monoxide production. Tissue homogenates were centrifuged and the 13,000g supernatants were incubated in septum-sealed vials with methemalbumin in the presence and absence of NADPH at 37 degrees C for 15 min. The reaction was terminated by quick-freezing to -78 degrees C and the amount of carbon monoxide released into the headspace was determined by gas chromatography with a reduction gas detector. The CO produced through mediation of NADPH is used as a measure of HO activity and is expressed as nanomoles of CO produced per hour per milligram protein. The method permits analysis of as little as 2 microliter normal rat tissue homogenate representing 0.4 mg liver tissue (approx 40 micrograms total protein). The assay rate is 10-15 duplicate samples per hour with a precision of 3% for sample (4.47 +/- 0.13 SD nmol CO/h/mg protein) and 6% for blank reactions (0.59 +/- 0.10 nmol CO/h/mg protein) for 10 microliter liver supernatant. Various reaction parameters were studied. The method was used to compare HO activity in several tissue homogenates from normal rats and rats treated with COCl2.     

Kidney and liver metallothioneins in rats after administration of an organic compound

Intubation of rats with alpha-mercapto-beta-(2-furyl)-acrylic acid (MFA) for 5 days at 50 mg/kg caused a 7-fold increase in kidney copper concentration, a 2-fold increase in kidney zinc concentration, and a 20% increase in liver zinc concentration. The proteins which bound the increased metals were purified and identified as metallothioneins by their amino acid compositions. Two isoforms were isolated from each organ. Renal thioneins appeared identical to counterpart hepatic apoproteins, but the former bound Cu and Zn in a 2:1 mole ratio and the latter bound only Zn. Kidney contained over 10 times more metallothionein per g of tissue than did liver. In rats previously administered MFA, injection of cadmium sulfate resulted in rapid displacement of liver metallothionein-bound Zn by Cd under conditions where minimal metallothionein was found in Cd-dosed animals not administered MFA. We conclude that MFA induces metallothionein biosynthesis in kidney and liver of normal rats; this is a novel effect for an organic compound.     

The effect of adlay oil on plasma lipids, insulin and leptin in rat.

This study was designed to investigate the effect of dietary adlay oil on plasma lipids, insulin and lipid peroxidation levels in rats. Twenty-four male Wistar rats fed diet containing adlay oil and cholesterol were studied for 4 weeks. The animals were divided into three groups: (1) 10% lard (control) group; (2) 5% lard + 5% adlay oil (5% adlay oil) group; and (3) 10% adlay oil group. Although there was no significant difference in body weight at the end of the feeding study, rats fed a diet containing adlay oil showed a significant decrease in adipose tissue weight and relative adipose weight. In addition, the rats fed the adlay oil showed significantly decreased low-density lipoprotein cholesterol (LDL-C), insulin, leptin and thiobarbituric acid reactive substance (TBARS) concentrations after 4 weeks of the feeding study. Although a significant decrease in total plasma cholesterol was observed in rats fed the 5% adlay oil diet, no significant difference was observed between the 10% adlay oil and control groups, and neither was a significant difference in liver TBARS concentration found between the dietary groups. Results from this study suggest that dietary adlay oil can reduce leptin, adipose tissue and LDL-C levels in rats.     

Thermogenic effects of dihydrocodeine in the rat

The object of this study was to assess the effects of dihydrocodeine on thermogenesis and brown adipose tissue activity in the rat from measurements of oxygen consumption and blood flow. Acute injection of dihydrocodeine tartrate (s.c.) stimulated resting oxygen consumption (VO2) in Sprague-Dawley rats in a dose-dependent manner (0.5-50 mg/kg), with a peak response (40-45% increase) occurring at 10-25 mg/kg. This effect was also observed in urethane-anaesthetized rats (although the effect was reduced) and in conscious animals following gastric intubation with the drug. Pretreatment of rats with either a beta-adrenergic antagonist (propranolol, 20 mg/kg), ACTH (4 g/kg), or an opiate antagonist (WIN44441-1, 2 mg/kg) significantly reduced the response to dihydrocodeine, whereas corticosterone injection (5 mg/kg) enhanced the effect. Surgical adrenalectomy or hypophysectomy (HYPX) almost completely abolished the thermogenic effect of dihydrocodeine. Dihydrocodeine also stimulated VO2 in lean (58% increase) and genetically obese Zucker rats (69% increase), and in both Zucker genotypes these responses were only slightly affected by HYPX, but enhanced in HYPX rats treated daily with corticosterone (1 mg/kg). Tissue blood flow, assessed from the distribution of radiolabelled microspheres, was unaffected in white adipose tissue, skeletal muscle, testes, kidney, brain, and liver (arterial supply) after a single injection of dihydrocodeine (25 mg/kg), but flow to interscapular and perirenal brown adipose tissue was increased by 9- to 10-fold. Surgical sympathectomy of brown adipose tissue prevented the increase in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of exercise and adrenal insufficiency on urea production in rats

Experiments on Wistar rats were designed to study the effect of exercise on urea production in the liver of intact and adrenalectomized rats. The urea production rate was assessed by the¹⁴C-urea content in liver tissue after administration of NaH¹⁴CO₃. In intact rats swimming caused increases in¹⁴C-urea content in the liver compared to the resting concentrations in intact control rats: by 45% after 30 min of swimming carrying an additional load of 10% body mass by, 35% after 3 h of swimming without an additional load and by 103% after 10 h of swimming. Concentrations of urea in liver and blood were elevated simultaneously. The specific activity of¹⁴C-urea did not change significantly as a result of the exercise performed. In adrenalectomized rats the basal rate of urea production was reduced by an insignificant amount, but swimming for 3 h resulted in a decrease in liver¹⁴C-urea (by 24%). The results confirmed the exercise-induced increase in urea production and indicated as essential role for adrenal hormones in this response.     

Heat Shock Preconditioning Reduces the Formation of 8-hydroxy-2′-deoxyguanosine and 4-hydroxy-2-nonenal Modified Proteins in Ischemia-reperfused Liver of Rats

Heat shock preconditioning (HSPC) is a promising strategy for providing ischemic tolerance. The objective of this study is to investigate the effectiveness of HSPC in preventing oxidative damage of cellular proteins and DNA during ischemia-reperfusion of the liver. Male Wistar rats were divided into a heat shock group (group HS) and control (group C). Forty-eight hours prior to ischemia, rats in group HS received HSPC at 42°C for 15 &#117 min. All rats received hepatic warm ischemia for 30 &#117 min and subsequent reperfusion. The formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG), 4-hydroxy-2-nonenal (HNE) modified proteins in liver tissue, survival rate of the animals, and changes in biochemical and histological parameters were compared between groups. Heat shock protein 72 was produced only in group HS. The 7-day survival of rats was significantly better in group HS (10/10) than in group C (5/10) ( p <0.01). The serum release of alanine aminotransferase ( n =10, p <0.01) and the concentration of adenosine triphosphate in liver tissue ( n =10, p <0.01) 40 &#117 min after reperfusion was significantly better in group HS than in group C. The formation of 8-OHdG in liver tissue measured by high-performance liquid chromatography was suppressed in group HS ( p <0.01). The production of HNE-modified proteins as determined by Western-blot analysis was also decreased in group HS. These results were also confirmed by immunohistochemical analysis. As determined by levels of 8-OHdG and HNE-modified proteins produced during ischemia-reperfusion of the liver, HSPC reduced the oxidative injury of cellular proteins and DNA in the liver tissue.     

Heat shock preconditioning reduces the formation of 8-hydroxy-2'-deoxyguanosine and 4-hydroxy-2-nonenal modified proteins in ischemia-reperfused liver of rats

Heat shock preconditioning (HSPC) is a promising strategy for providing ischemic tolerance. The objective of this study is to investigate the effectiveness of HSPC in preventing oxidative damage of cellular proteins and DNA during ischemia-reperfusion of the liver. Male Wistar rats were divided into a heat shock group (group HS) and control (group C). Forty-eight hours prior to ischemia, rats in group HS received HSPC at 42 degrees C for 15 min. All rats received hepatic warm ischemia for 30min and subsequent reperfusion. The formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG), 4-hydroxy-2-nonenal (HNE) modified proteins in liver tissue, survival rate of the animals, and changes in biochemical and histological parameters were compared between groups. Heat shock protein 72 was produced only in group HS. The 7-day survival of rats was significantly better in group HS (10/10) than in group C (5/10) (p < 0.01). The serum release of alanine aminotransferase (n = 10, p < 0.01) and the concentration of adenosine triphosphate in liver tissue (n = 10, p < 0.01) 40min after reperfusion was significantly better in group HS than in group C. The formation of 8-OHdG in liver tissue measured by high-performance liquid chromatography was suppressed in group HS (p < 0.01). The production of HNE-modified proteins as determined by Western-blot analysis was also decreased in group HS. These results were also confirmed by immunohistochemical analysis. As determined by levels of 8-OHdG and HNE-modified proteins produced during ischemia-reperfusion of the liver, HSPC reduced the oxidative injury of cellular proteins and DNA in the liver tissue.     

Content of liver and brain ubiquinol-9 and ubiquinol-10 after chronic ethanol intake in rats subjected to two levels of dietary alpha-tocopherol

To assess the effect of chronic ethanol ingestion in the content of the reduced forms of coenzymes Q9 (ubiquinol-9) and Q10 (ubiquinol-10) as a factor contributing to oxidative stress in liver and brain, male Wistar rats were fed ad libitum a basal diet containing either 10 or 2.5 mg alpha-tocopherol/100 g diet (controls), or the same basal diet plus a 32% ethanol-25% sucrose solution. After three months treatment, ethanol chronically-treated rats showed identical growth rates to the isocalorically pair-fed controls, irrespectively of alpha-tocopherol dietary level. Lowering dietary alpha-tocopherol led to a decreased content of this vitamin in the liver and brain of control rats, without changes in that of ubiquinol-9, and increased levels of hepatic ubiquinol-10 and total glutathione (tGSH), accompanied by a decrease in brain tGSH. At the two levels of dietary alpha-tocopherol, ethanol treatment significantly decreased the content of hepatic alpha-tocopherol and ubiquinols 9 and 10. This effect was significantly greater at 10 mg alpha-tocopherol/100 g diet than at 2.5, whereas those of tGSH were significantly elevated by 43% and 9%, respectively. Chronic ethanol intake did not alter the content of brain alpha-tocopherol and tGSH, whereas those of ubiquinol-9 were significantly lowered by 20% and 14% in rats subjected to 10 and 2.5 mg alpha-tocopherol/100 g diet, respectively. It is concluded that chronic ethanol intake at two levels of dietary alpha-tocopherol induces a depletion of hepatic alpha-tocopherol and ubiquinols 9 and 10, thus contributing to ethanol-induced oxidative stress in the liver tissue. This effect of ethanol is dependent upon the dietary level of alpha-tocopherol, involves a compensatory enhancement in hepatic tGSH availability, and is not observed in the brain tissue, probably due to its limited capacity for ethanol biotransformation and glutathione synthesis.     

Role of maternal tissue in the synthesis of polyunsaturated fatty acids in response to a lipid-deficient diet during pregnancy and lactation in rats

During pregnancy and lactation, metabolic adaptations involve changes in expression of desaturases and elongases (Elovl2 and Elovl5) in the mammary gland and liver for the synthesis of long-chain polyunsaturated fatty acids (LC-PUFAs) such as arachidonic acid (AA) required for fetal and postnatal growth. Adipose tissue is a pool of LC-PUFAs. The response of adipose tissue for the synthesis of these fatty acids in a lipid-deficient diet of dams is unknown. The aim of this study was to explore the role of maternal tissue in the synthesis of LC-PUFAs in rats fed a low-lipid diet during pregnancy and lactation. Fatty acid composition (indicative of enzymatic activity) and gene expression of encoding enzymes for fatty acid synthesis were measured in liver, mammary gland and adipose tissue in rats fed a low-lipid diet. Gene expression of desaturases, elongases, fatty acid synthase (Fasn) and their regulator Srebf-1c was increased in the mammary gland, liver and adipose tissue of rats fed a low-lipid diet compared with rats from the adequate-lipid diet group throughout pregnancy and lactation. Genes with the highest (P < 0.05) expression in the mammary gland, liver and adipose tissue were Elovl5 (1333%), Fads2 (490%) and Fasn (6608%), respectively, in a low-lipid diet than in adequate-lipid diet. The percentage of AA in the mammary gland was similar between the low-lipid diet and adequate-lipid diet groups during the second stage of pregnancy and during lactation. The percentage of monounsaturated and saturated fatty acids was significantly (P < 0.05) increased throughout pregnancy and lactation in all tissues in rats fed a low-lipid diet than in rats fed an adequate-lipid diet. Results suggest that maternal metabolic adaptations used to compensate for lipid-deficient diet during pregnancy and lactation include increased expression of genes involved in LC-PUFAs synthesis in a stage- and tissue-specific manner and elevated lipogenic activity (saturated and monounsaturated fatty acid synthesis) of maternal tissues including adipose tissue.     

育阴软肝颗粒剂对肝纤维化大鼠TGF-β1表达的影响

目的：观测育阴软肝颗粒剂对大鼠肝纤维化模型的防治作用及对转化生长因子-β1（TGF-β1）表达的影响。方法：将Wistar大鼠分为6组（n=10）,注射四氯化碳、饲以高脂饲料并饮用20%乙醇6周复制肝纤维化大鼠模型,经6.2~24.8 g/kg育阴软肝颗粒剂干预（qd）6周后,测定肝纤维化大鼠血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）活性、透明质酸（HA）、Ⅲ型前胶原（PCⅢ）、Ⅳ型胶原（C-Ⅳ）及板层素（LN）含量,观测肝组织病理学及肝组织TGF-β1表达的变化,对育阴软肝颗粒剂防治肝纤维作用及机制进行研究。结果：实验第7周,模型组大鼠肝组织出现明显的纤维化病变（P<0.01）;与模型组比较,6.2~24.8g/kg的育阴软肝颗粒剂能明显降低肝指数以及血清ALT、AST活性与HA、PCⅢ、C-Ⅳ、LN含量,缓解肝组织纤维化病理变化,抑制纤维化肝组织TGF-β1的表达（P<0.05,0.01）。结论：育阴软肝颗粒剂对多因素复制肝纤维化大鼠造模具有明显的治疗作用,而抑制TGF-β1的表达可能是其作用机制之一。     

Dietary conjugated linoleic acid has limited effects on tissue protein anabolism in sedentary and exercising adult rats

The effects of conjugated linoleic acid isomers (CLA) and endurance training on lean body mass are expected to result from their action on tissue protein metabolism. The aim of this study was to analyze their effects on protein metabolism in 2 muscles, the small intestine and liver of adult rats. Four-month-old male Wistar rats were fed diets containing either no CLA, cis-9, trans-11 CLA isomer (1 g.100 g(-1)), trans-10, cis-12 CLA isomer (1 g.100 g(-1)) or both isomers (1 g.100 g(-1) each) for 6 weeks. Half of the rats were subjected to endurance training by running on a treadmill. At the end of this period, the rats were injected with a flooding dose of (13)C-valine to determine protein synthesis rates in the post-absorptive (experiment 1) and in the post-prandial (experiment 2) states. No effect of CLA or endurance training were detected in the small intestine. Training reduced food intake and protein synthesis rates in the liver but no effect was found on the protein synthesis rates in muscles. In the post-absorptive state, protein synthesis rate was increased by feeding the trans-10, cis-12 CLA isomer alone in the liver (+9%) or in combination with the cis-9, trans-11 isomer in the gastrocnemius (+30%), mostly in sedentary rats. In the post-prandial state, the cis-9, trans-11 CLA isomer tended to reduce the protein synthesis rate in the gastrocnemius muscle. However, no effect of CLA was found on muscle protein amounts. In conclusion, CLA isomers would have limited but differential effects on tissue protein metabolism in adult rats.     

Synthesis and preliminary evaluation of mono-[123I]iodohypericin monocarboxylic acid as a necrosis avid imaging agent

Hypericin monocarboxylic acid was synthesized in an overall yield of 25% in four steps and radiolabelled with iodine-123 in good yield (>75%). The resulting mono-[(123)I]iodohypericin monocarboxylic acid was evaluated in normal mice and in rats with ethanol induced liver necrosis. In this model, tracer concentration in necrotic liver tissue was 14 times higher than in the viable liver tissue as quantified by autoradiography at 24h post injection. The results indicate the feasibility of visualization of necrotic tissue with the novel tracer.