四氯化碳两种途径亚急性实验染毒时某些肝酶指标的对比研究

本文用CCl_41.356g/kg和5.87g/kg分别对大鼠进行皮下和呼吸道静式染毒,为期8周亚急性中毒试验,研究临床常用血清肝酶指标的变化。结果发现:CCl_4除使大鼠体重增长减慢外,第1周起出现肝细胞脂变、浊肿,进而坏死、纤维增生和肝硬化;肝糖元及SHD酶活性减少或消失,G-6-P酶活性先升高后降低的病理形态和组织化学的改变。与此同时或稍后出现SGPT和SGOT活性升高,持续至第8周。停药两周,肝病理改变趋于恢复,SGPT和SGOT活性也恢复至接近正常,两肝酶与病理改变相平行。AKP酶活性第4周后才升高;ChE酶似有先升高后降低趋势,但无明显差异性;γ-GT酶变化不规则。提示CCl_4亚急性中毒时,SGPT和SGOT酶活性升高与肝损关系较密切,可作临床早期诊断指标。血清AKP和ChE酶亦一定程度反映肝损的发展情况,可供作临床观察病情发展的辅助指标。     

氯乙烯染毒大鼠DNA损伤与肝脏某些生化指标的变化

目的　研究氯乙烯 (VCM)对大鼠肝细胞和血淋巴细胞DNA的损伤作用 ,及肝脏某些生化指标的变化。方法　DNA损伤采用单细胞凝胶电泳 (彗星实验 )法 ,代谢酶活性采用分光光度法 ,肝功能测定使用自动生化分析仪。结果　彗星发生率染毒组显著高于对照组 ,肝细胞和血淋巴细胞彗星发生率显著相关。结论　VCM可导致大鼠肝细胞和血淋巴细胞DNA发生损伤 ,且存在剂量 效应 反应关系。     

二月桂酸二丁基锡对大鼠肝脏毒性作用

目的用二月桂酸二丁基锡（DBTD）染毒大鼠，探讨DBTD对大鼠肝脏及血清中酶活性的影响。方法选踺康成年大鼠28只。随机分为0，5，10，20mg／kg4个剂量组，每组7只动物，用DBTD灌胃染毒5周后处死动物，测定血清中碱性磷酸酶（ALP）、谷丙转氨酶（GPT）、γ-谷氨酰基转移酶（GGT）、肝组织中酸性磷酸酶（ACP）、碱性磷酸酶（AKP）、乳酸脱氢酶（LDH）活性及肝脏中锡含量。结果各剂量组大鼠肝脏中锡含量，肝组织中ACP、AKP、LDH。血清中ALP、GGT、GPT活性明显高于对照组（P〈0．01，P〈0．05）。结论DBTD可在肝组织中蓄积，具有肝毒性．可影响忏审酶的活幛两阡的下皆曲能     

饮用水有机提取物致大鼠肝脏损伤中GSTs活性及其编码基因表达的变化

[目的]观察饮用水有机提取物对大鼠肝脏谷胱甘肽-S-转移酶(glutathione-S-transferase,GSTs)活性及谷胱甘肽-S-转移酶A1(GSTA1)基因m RNA和蛋白表达的影响,探讨其在饮用水有机提取物肝脏损伤中作用。[方法]采用固相萃取法提取水样中有机污染物,50只SD大鼠随机分成5组,分别为空白对照组、溶剂对照组(玉米油)和低、中、高3个染毒组(剂量分别为每天5、20、80 L/kg·bw),进行经口灌胃染毒12周。分光光度法检测GSTs的活性,实时荧光定量聚合酶链反应法和Western blot法分别检测GSTA1基因的m RNA和蛋白质表达水平,同时检测肝功能各指标。[结果](1)大鼠肝脏GSTs酶活性:与空白对照、溶剂对照及低剂量组相比,中剂量[(50.66±5.62)U/mg蛋白]和高剂量组[(39.80±12.95)U/mg蛋白]的GSTs酶活性升高(P<0.05);与中剂量组相比,高剂量组GSTs的酶活性则明显降低(P<0.05)。(2)GSTA1的m RNA及蛋白表达水平:中、高剂量组高于空白对照组、溶剂对照及低剂量组(P<0.05);而与中剂量组相比,高剂量组GSTA1的m RNA表达水平下降(P<0.05)。Western blot检测结果显示,随染毒剂量的增加,GSTA1蛋白表达呈先升高后降低的趋势,与空白对照、溶剂对照及低剂量组比较,中、高剂量组的升高,差异具有统计学意义(P<0.05);而与中剂量组比较,高剂量GSTA1的蛋白表达则下降(P<0.05)。(3)肝功能指标:与对照组比较,血清胆碱酯酶(CHE)在中、高剂量染毒组升高,差异均具有统计学意义(P<0.05);丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转换酶(AST)则仅在高剂量组升高(P<0.05)。总蛋白(TP)和白蛋白(ALB)在高剂量组下降(P<0.05)。GSTA1蛋白表达、GSTs活性与染毒大鼠肝脏CHE水平均呈正相关关系(r=0.490 5,r=0.685 2;P<0.05)。[结论]在本实验条件下,饮用水有机提取物较高剂量染毒可上调大鼠肝脏GSTA1的m RNA及蛋白质表达水平,调控GSTs活性改变,从而导致大鼠肝细胞对毒物的易感性增强,肝损伤加重。     

三硝基甲苯(TNT)对大鼠毒作用的实验研究

本文报道了TNT对大鼠毒作用所引起主要脏器的病理改变和某些生化指标的变化。对肝组织作了电镜观察。染毒早期可见肝内质网扩张。亚急性中毒肝线粒体变性和内质网扩张成小泡状。光镜检查见肝细胞浊肿、嗜酸变和嗜酸小体形成。生化指标测定中,LDH_1和LDH_2升高,提示TNT除作用于肝脏外,可能对心肌亦有作用。200mg/kg染毒一周,大鼠睾丸即出现明显的病理改变,因此,睾丸对TNT也是敏感的器官之一。     

三硝基甲苯(TNT)对大鼠毒作用的实验研究

本文报道了TNT对大鼠毒作用所引起主要脏器的病理改变和某些生化指标的变化.对肝组织作了电镜观察.染毒早期可见肝内质网扩张.亚急性中毒肝线粒体变性和内质网扩张成小泡状.光镜检查见肝细胞浊肿、嗜酸变和嗜酸小体形成.生化指标测定中,LDH_1和LDH_2升高,提示TNT除作用于肝脏外,可能对心肌亦有作用.200mg/kg染毒一周,大鼠睾丸即出现明显的病理改变,因此,睾丸对TNT也是敏感的器官之一.     

茴香提取液对小鼠酒精性肝损伤的保护作用

目的探究茴香提取液对小鼠酒精性肝损伤的保护作用。方法用56度北京红星二锅头白酒建立小鼠酒精性肝损伤模型,用茴香进行干预,30 d后,眼球采血测血清TG(甘油三酯)、TC(总胆固醇)水平和ALT(谷丙转氨酶)、AST(谷草转氨酶)活性,测量体重和肝脏称重,计算肝指数;取肝组织匀浆液测肝组织TG、TC、MDA(丙二醛)、GSH(谷胱甘肽)的含量和ADH(乙醇脱氢酶)、SOD(超氧化物歧化酶)活性;HE染色,观察肝脏组织形态学的改变。结果与正常组相比,模型组肝指数、血清AST、ALT酶活性、肝组织MDA、TG、TC水平增高(P0.01),肝组织GSH水平和ADH、SOD酶活性有降低(P0.01,0.05),肝细胞形态不规则,呈弥漫性水样变,有少量肝细胞膜溶解,细胞核消失。与模型组相比,茴香中、高剂量组肝指数、肝组织TC、MDA水平、血液TG水平降低(P0.05,0.01);茴香高剂量组AST和ALT酶活性、肝组织TG水平降低(P0.05,0.01);茴香高剂量组ADH、SOD活性,GSH水平均升高,差异有统计学意义(P0.05,0.01);肝组织病理变化明显减轻,以茴香高剂组改善较为明显。结论茴香可能通过提高机体对自由基的防御能力和提高乙醇脱氢酶活性加快乙醇代谢而减轻酒精对肝脏的损伤。     

4种血清酶在三硝基甲苯染毒致大鼠肝损伤中的变化及意义

[目的]观察三硝基甲苯(TNT)染毒致大鼠肝损伤时血清乳酸脱氢酶(LDH)、谷氨酸氨基移换酶(ALT)、天门冬酸氨基移换酶(AST)和碱性磷酸酶(ALP)的活力变化情况,并探讨其意义。[方法]以50、100和200mg/kg体重剂量的TNT对大鼠每天一次经口染毒,分别于染毒2、4、6和8周后处死,测定血和肝组织TNT代谢产物2,6-二硝基-4-氨基甲苯(DNAT)水平、血靛青绿(ICG)10min滞留率(ICG_(R10))和血清LDH、ALT、AST、ALP的变化情况。[结果]TNT染毒大鼠血和肝组织DNAT均比对照组有明显升高,TNT染毒剂量与大鼠血清或肝组织DNAT呈显著性相关(P<0.01),血清与肝组织DNAT呈显著性相关(P<0.01);各TNT染毒组大鼠血清ICG_(R10)明显高于对照组。TNT高剂量染毒组大鼠血清LDH、ALT、AST和ALP活力有所降低,其他剂量组与对照组相比未见显著性变化;血清或肝组织DNAT与血清LDH呈显著性负相关(P<0.05或0.01),与ALT、AST和ALP均负相关,但未见显著性(P>0.05)。[结论]血清LDH、ALT、AST和ALP指标对TNT染毒诱导的大鼠肝损伤的反应并不敏感,似与TNT代谢产物DNAT对血清4种酶活力可能具有的一定抑制作用有关。     

间二硝基苯染毒对大鼠血清生化指标的影响

目的探讨间二硝基苯（ｍ－ＤＮＢ）染毒对肝、肾及代谢方向的影响。方法用ＨＩＴＡＣＨＩ７１５０型全自动生化分析仪分析ｍ－ＤＮＢ染毒大鼠血清常规生化指标。结果ｍ－ＤＮＢ染毒大鼠血清胆红毒和肾功能指标的改变相对比较突出,而多数血清酶、脂质和载脂蛋白等指标的影响均较小。结论血清胆红素、肌酐（ＣＲＥ）和尿酸（ＵＡ）可能是ｍ－ＤＮＢ所致的肝脏和肾脏毒性的敏感指标     

海参和海星脑苷脂对大鼠急性肝损伤影响的比较研究

目的比较海参和海星脑苷脂对四氯化碳致大鼠急性肝损伤的影响。方法 24只大鼠按体重随机分为4组,分正常组、模型组、海参脑苷脂组(SCC)和海星脑苷脂组(SF),分别腹腔注射相应受试物10天,并于实验进行第7天开始利用四氯化碳(CCl4)建立急性肝损伤模型。测定了血清肝损伤指示酶活性和肝脏氧化应激水平以及肝脂含量,并观察了肝脏形态学变化,进行了DNA电泳分析。结果与正常组比,模型组大鼠血清中肝损伤指示酶活性均显著升高,肝脏脂质大量蓄积,肝脏中丙二醛(MDA)和一氧化氮(NO)含量显著增加,谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活性显著降低,肝脏呈现明显病变,肝细胞大量坏死。海参脑苷脂组血清乳酸脱氢酶(LDH)、丙氨酸转氨酶(或称谷丙转氨酶ALT or GPT)、碱性磷酸酶(AKP)和天冬氨酸转氨酶(或称谷草转氨酶,AST or GOT)活性和肝脏MDA、NO含量以及肝脂含量相比模型组显著降低,GSH-Px和CAT活性显著升高,肝组织病变和肝细胞坏死状况明显改善,而海星脑苷脂组血清酶活和肝脏氧化应激水平变化不显著,肝脏脂肪含量显著降低。肝组织病变和肝细胞坏死改善效果相比海参脑苷脂组略差。结论海参脑苷脂对四氯化碳引发大鼠急性肝损伤的机制可能与其能够清除自由基,降低过氧化物,调节脂质代谢等作用有关,而海星脑苷脂对大鼠肝脏脂质蓄积表现出良好的改善效果,但其对肝损伤的作用机制仍有待深入研究。     

氯乙烯致大鼠DNA损伤与肝代谢酶活性动态变化的研究

[目的]研究氯乙烯(VC)对大鼠肝细胞和外周血淋巴细胞DNA的损伤作用，及对VC代谢酶[谷胱甘肽硫转移酶(GST)、细胞色素P4502E1(CYP2E1)、乙醇脱氢酶(ADH)和乙醛脱氢酶(ALDH)]活性的影响；探索VC所致损伤的早期敏感检测指标。[方法]大鼠染毒12周，分别在第3、6、9和12周处死动物，DNA损伤采用单细胞凝胶电泳(彗星试验)法，代谢酶活性测定采用分光光度法。[结果]彗星细胞数目随染毒剂量和染毒时间的增加而增加，肝细胞DNA损伤细胞百分率第12周中剂量组和高剂量组分别为12.38％和17.88％，外周血淋巴细胞DNA损伤细胞百分率第3周高剂量组为7．33％，第12周中剂量组和高剂量组分别为16．25％和28、25％，均显著高于相应对照组，彗星细胞发生率与VC染毒剂量间存在显著相关关系。ALDH和CYP2E1活性随染毒时间和染毒剂量的增加发生改变，差异具显著性。肝细胞DNA损伤与CYP2EI活性相关。[结论]VC可导致肝细胞和外周血淋巴细胞DNA发生损伤，且存在剂量．反应和时间一效应关系；VC致肝细胞DNA损伤与CYP2E1代谢酶活性相关。彗星细胞率可作为VC所致肝脏损伤的早期检测指标。     

氯乙烯致大鼠肝细胞DNA损伤与DNA修复基因表达

目的　研究氯乙烯 (VCM)对大鼠肝细胞DNA的损伤作用 ,及对DNA损伤修复酶 [O6 甲基鸟嘌呤 DNA甲基转移酶 (MGMT)、X线修复交叉互补基团 1(XRCC1)和X线修复交叉互补基团 3(XRCC3) ]表达的影响 ;探索VCM所致DNA损伤的修复机制。方法　采用腹腔注射VCM染毒 ,实验组按不同染毒剂量分为 3个剂量组 ,分别为低剂量 5mg kg、中剂量 10mg kg和高剂量 2 0mg kg ,染毒12周 ,以单细胞凝胶电泳 (彗星试验 )测DNA损伤 ,免疫组化法测DNA损伤修复酶的表达。结果　低、中和高剂量组大鼠肝细胞DNA损伤细胞百分率分别为 11.75 %、12 .38%和 17.6 3% ,均高于对照组(5 .6 7% ) ,且中、高剂量与对照组比较 ,差异有显著性 (P <0 .0 5 ,P <0 .0 1)。MGMT和XRCC1表达随染毒剂量增加而减少 ,而XRCC3的表达随染毒剂量的增加而增加。VCM致DNA损伤与XRCC3表达有相关关系 (r=0 .4 38,P =0 .0 6 7)。结论　VCM可导致肝细胞DNA发生损伤 ,且存在剂量 -反应关系 ;DNA损伤修复酶参与修复VCM所致的DNA损伤。     

Effect of dietary cholesterol on hepatic lipogenesis and plasma insulin and free fatty acid levels in rats.

In order to further investigate the metabolic alterations in the liver of cholesterol-fed rats, the following parameters were determined: (a) the activities of hepatic glucose-6-phosphate dehydrogenase, NADP-malate dehydrogenase, citrate cleavage enzyme, acetyl CoC carboxylase, and fatty acid synthetase; (b) the rate of hepatic fatty acids synthesis in vivo or in vitro; and (c) the concentration of immunoreactive insulin, free fatty acids, and glucose in the plasma. The experimental diets usually contained 1.5% cholesterol and 0.5% cholic acid. Cholesterol feeding resulted in a three- to fourfold decrease in the activities of hepatic glucose-6-phosphate dehydrogenase, NADP-malate dehydrogenase, and citrate cleavage enzyme and up to a two-fold decrease in the activities of acetyl CoA carboxylase and fatty acid synthetase. The rate of fatty acid synthesis was not sifnigicantly decreased when rats were fed the cholesterol-supplemented diets for only 2 to 4 weeks, despite marked decreases in the activities of the lipogenic enzymes. But when cholesterol feeding was continued for periods longer than 5 weeks, there was a significant decrease in the rate of fatty acid synthesis in the liver. Cholesterol feeding decreased the levels of circulating insulin and elevated plasma free fatty acid levels. Plasma glucose levels were not significantly changed. Cholesterol feeding can result in a wide range of metabolic alterations. These metabolic alterations may have some impact on the development of hypercholesterolemic-related metabolic disorders.     

Effect of pyridoxine deficiency and prednisolone on beta-alanine-oxoglutarate aminotransferase and D-3-aminoisobutyrate aminotransferase in rat liver and kidney

beta-Alanine-oxoglutarate aminotransferase (beta-Ala-TI) was found to be distributed mainly in liver, brain, kidney, and testis (decreasing order of enzyme activity in the rat). D-3-Aminoisobutyrate aminotransferase (beta-Ala-T II) was distributed in kidney and liver. Both beta-Ala-T I and beta-Ala-T II were localized in the mitochondrial fraction in rat kidney. beta-Ala-T I in the liver of rats fed on pyridoxine-deficient or control diets was induced by injecting with prednisolone, while beta-Ala-T II in the liver of these rats was unaffected by prednisolone injection. The activities of beta-Ala-T I and beta-Ala-T II in the liver of rats fed on pyridoxine deficient diet did not change. However, in kidney, pyridoxine deficiency suppressed both enzyme activities, while treatment with prednisolone did not induce either enzyme. The ratios of the apo- to holo-enzyme for beta-Ala-T I and beta-Ala-T II in control rat kidney were 1.04 and 0.11, respectively. The values increased to 2.69 and 1.53, respectively, in pyridoxine-deficient rat kidney. These experiments indicate that pyridoxine deficiency and prednisolone affect the activities of beta-alanine degrading enzymes, but that the degree is different between liver and kidney.     

Biochemical effects of vepacide (from Azadirachta indica) on Wistar rats during subchronic exposure

We investigated the effect of Vepacide (from Azadirachta indica), a neem-based pesticide, on acid (AcP) and alkaline (AkP) phosphatase in different tissues of male and female albino Wistar rats. Subchronic doses of Vepacide in coconut oil (80, 160, and 320 mg/kg; maximum volume of 0.2 mL) were administered orally for 45 or 90 days. The administration of Vepacide resulted in a significant increase in AcP and AkP in serum, kidney, lung, and liver tissue (AkP only in liver), whereas a significant decrease of AcP in liver was observed in male and female rats after 45 and 90 days of treatment with moderate and high doses. The alterations in serum, liver, kidney, and lung tissues of both male and female rats caused by this compound were statistically significant, and the changes were also dose and time dependent. The alterations in male rats were not statistically significant when compared with female rats, indicating that there were no sexual differences. The withdrawal study (28 days post-treatment) revealed significant recovery, indicating reversal of the toxic symptoms once the toxicant was removed. There was a high degree of positive correlation between results for serum as compared to those for kidney, lung, and liver (AkP only for liver). However, there was a high negative correlation between AcP results for serum as compared with those for liver. The alterations in these enzymes indicated that lung tissue was the most susceptible, followed by liver and kidney. AcP and AkP are marker enzymes, and their increase in serum, with parallel increases in different tissues, might be due to the increased permeability of plasma membranes. The decrease in liver AcP may be due to the necrosis of cellular tissues. The changes observed in these enzyme activities could be useful as biomarkers of exposure to Vepacide.     

Influence of Ramadan-type fasting on enzymes of carbohydrate metabolism and brush border membrane in small intestine and liver of rat used as a model

During Ramadan, Muslims the world over abstain from food and water from dawn to sunset for a month. We hypothesised that this unique model of prolonged intermittent fasting would result in specific intestinal and liver metabolic adaptations and hence alter metabolic activities. The effect of Ramadan-type fasting was studied on enzymes of carbohydrate metabolism and the brush border membrane of intestine and liver from rat used as a model. Rats were fasted (12 h) and then refed (12 h) daily for 30 d, as practised by Muslims during Ramadan. Ramadan-type fasting caused a significant decline in serum glucose, cholesterol and lactate dehydrogenase activity, whereas inorganic phosphate increased but blood urea N was not changed. Fasting resulted in increased activities of intestinal lactate (+34%), isocitrate (+63%), succinate (+83%) and malate (+106%) dehydrogenases, fructose 1,6-bisphosphatase (+17%) and glucose-6-phosphatase (+22%). Liver lactate dehydrogenase, malate dehydrogenase, glucose-6-phosphatase and fructose 1,6-bisphosphatase activities were also enhanced. However, the activities of glucose-6-phosphate dehydrogenase and malic enzyme fell significantly in the intestine but increased in liver. Although the activities of alkaline phosphatase, gamma-glutamyl transpeptidase and sucrase decreased in mucosal homogenates and brush border membrane, those of liver alkaline phosphatase, gamma-glutamyl transpeptidase and leucine aminopeptidase significantly increased. These changes were due to a respective decrease and increase of the maximal velocities of the enzyme reactions. Ramadan-type fasting caused similar effects whether the rats fasted with a daytime or night-time feeding schedule. The present results show a tremendous adaptation capacity of both liver and intestinal metabolic activities with Ramadan-type fasting in rats used as a model for Ramadan fasting in people.     

Liver function assessment in workers exposed to vinyl chloride

Objective: To investigate liver function in vinyl chloride workers and assess its relation with current/past occupational exposure to vinyl chloride monomer (VCM). Methods: A medical examination including the execution of liver function tests (LFTs) and liver ultrasonography was executed in a group of 757 workers with a long-standing service in the production of VCM/polyvinylchloride (PVC). Cumulative and maximum VCM exposures were calculated. History of viral hepatitis and alcohol intake were carefully investigated. Regression analysis explored the association between abnormal LFTs and a group of possible determinants (VCM cumulative and maximum exposure, BMI, age, history of viral hepatitis, alcohol and triglyceride levels). Also, synergistic effect between VCM and a history of hepatitis was analysed, as well as the possible association between VCM exposure and aspartate aminotransferase/alanine amino transferase (AST/ALT) ratio >1. Distribution of abnormal LFTs was also assessed in relation to the results provided by liver ultrasonography. Results: The most frequently abnormal serum parameters were, in decreasing order: total cholesterol (27.3%), triglycerides (12.2%), total bilirubin (9.1%), gamma glutamil transpeptidase (GGT; 9.0%) and ALT (8.2%). The AST/ALT ratio >1 was present in 28.1% of workers. Abnormal LFTs were not found to be associated with current or past VCM exposure. High ALT resulted positively associated with BMI, AST with alcohol intake, GGT with alcohol intake and triglycerides. No synergistic effect on LFTs of exposure to VCM and a history of hepatitis was observed. The AST/ALT ratio >1 was not found to be associated with VCM exposure. The prevalence of abnormal LFTs was higher in case of liver steatosis (ALT) or periportal fibrosis (GGT), but not in case of pure hepatomegaly, as documented by ultrasonography. Conclusions: Liver function assessment only including LFTs is not able to detect VCM-induced liver damage, but reveals alterations due to non-occupational factors, such as dietary and/or metabolic disfunctions. The LFTs are however of importance to detect conditions that could recommend avoidance of exposure to VCM and are useful for medical counselling and health promotion purposes.     

Influence of Ramadan-type fasting on carbohydrate metabolism, brush border membrane enzymes and phosphate transport in rat kidney used as a model

Ramadan fasting is a unique model of fasting in which Muslims the world over abstain from food and water from dawn to sunset for 1 month. We hypothesized that this model of prolonged intermittent fasting would result in specific adaptive alterations in rat kidney to keep a positive balance of metabolites and inorganic phosphate (Pi). The effect of Ramadan-type fasting was studied on enzymes of carbohydrate metabolism and brush border membrane (BBM) and BBM uptake of 32Pi in different renal tissue zones in the rat model. Rats were fasted (12 h) and then re-fed (12 h) daily for 30 d similar to human Ramadan fasting. Ramadan-type fasting resulted in increased serum Pi and phospholipids, whereas Pi clearance decreased. Serum creatinine and its clearance were not affected. Fasting caused a significant decrease in the activities of lactate and malate dehydrogenases, glucose-6-phosphatase and fructose-1,6-bisphosphatase, both in the renal cortex and medulla. However, the activity of glucose-6-phosphate dehydrogenase profoundly increased but that of malic enzyme decreased. The activities of alkaline phosphatase and gamma-glutamyl transpeptidase in BBM decreased, whereas transport of 32Pi significantly increased. The decrease in enzyme activities and increase in 32Pi transport were due to alterations of both maximal velocities and relative affinities. The results indicate that Ramadan-type fasting caused specific metabolic alterations with enhanced Pi conservation in different kidney tissues in a rat model used for Ramadan fasting in man.     

Effect of diet composition and ration size on key enzyme activities of glycolysis-gluconeogenesis, the pentose phosphate pathway and amino acid metabolism in liver of gilthead sea bream (Sparus aurata)

The effects of diet composition and ration size on the activities of key enzymes involved in intermediary metabolism were studied in the liver of gilthead sea bream (Sparus aurata). High-carbohydrate, low-protein diets stimulated 6-phosphofructo 1-kinase (EC 2.7.1.11), pyruvate kinase (EC 2.7.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and 6-phosphogluconate dehydrogenase (EC 1.1.1.44) enzyme activities, while they decreased alanine aminotransferase (EC 2.6.1.2) activity. A high degree of correlation was found between food ration size and the activity of the enzymes 6-phosphofructo 1-kinase, pyruvate kinase, glucose-6-phosphate dehydrogenase (positive correlations) and fructose-1,6-bisphosphatase (EC 3.1.3.11) (negative correlation). These correlations matched well with the high correlation also found between ration size and growth rate in starved fish refed for 22 d. Limited feeding (5 g/kg body weight) for 22 d decreased the activities of the key enzymes for glycolysis and lipogenesis, and alanine aminotransferase activity. The findings presented here indicate a high level of metabolic adaptation to both diet type and ration size. In particular, adaptation of enzyme activities to the consumption of a diet with a high carbohydrate level suggests that a carnivorous fish like Sparus aurata can tolerate partial replacement of protein by carbohydrate in the commercial diets supplied in culture. The relationship between enzyme activities, ration size and fish growth indicates that the enzymes quickly respond to dietary manipulations of cultured fish.