纳米氧化镍致大鼠肺毒性实验研究

目的探讨纳米氧化镍急性染毒致大鼠急性肺毒性的研究。方法将50只Wistar大鼠,雌雄各半,按体质量(180~220 g)分为5组,分别为0.9%氯化钠注射液对照组、微米氧化镍对照组(20 mg/ml)及纳米氧化镍(0.8、4、20 mg/ml)组。以非暴露式气管滴注法染毒,3 d 1次,染尘15 d后,腹主动脉抽血处死。分别对肺泡灌洗液和血清中总蛋白、白蛋白、碱性磷酸酶、酸性磷酸酶、乳酸脱氢酶的含量进行检测。结果大鼠支气管肺泡灌洗液中总蛋白含量、白蛋白含量、乳酸脱氢酶活力、碱性磷酸酶活力和酸性磷酸酶活力与0.9%氯化钠注射液对照组相比,纳米氧化镍中、高剂量组均升高且差异有统计学意义(P<0.05),各剂量组血清中总蛋白、白蛋白、碱性磷酸酶、酸性磷酸酶、乳酸脱氢酶水平的变化与对照组比较差异无统计学意义(P>0.05),纳米染毒剂量组之间的差异无统计学意义(P>0.05),同等剂量纳米与微米染毒组间的差异也无统计学意义(P>0.05)。结论纳米氧化镍可能对大鼠肺组织有急性毒性,且有剂量效应关系。     

BD-77雾化吸入给药对肺炎支原体感染小鼠的治疗作用

目的 评价BD-77雾化吸入给药对肺炎支原体肺炎小鼠模型的治疗作用。方法Balb/c小鼠按照体质量随机分为正常对照组、模型对照组、阿奇霉素对照组(42 mg·kg^-1·d^-1)、BD-77高剂量组(75 mg·mL^-1,雾化15 min)、BD-77低剂量组(37.5 mg·mL^-1,雾化15 min)。以肺炎支原体滴鼻感染建立小鼠支原体肺炎模型,雾化给药4 d后,通过小鼠体重及肺重计算肺指数和肺指数抑制率,酶联免疫吸附试验(ELISA)检测肺组织中白介素-6(IL-6)、白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)含量及血清中C反应蛋白(CRP)水平,苏木精-伊红(HE)染色评估小鼠肺组织病理学变化,全面评价BD-77对小鼠支原体肺炎的治疗作用。结果BD-77 2个剂量组雾化吸入给药15 min均可显著降低小鼠肺指数,减轻肺部炎症病变,降低肺组织中IL-6、IL-1β、TNF-α含量及血清CRP水平。结论BD-77雾化吸入可治疗支原体感染小鼠肺炎,本研究为BD-77开发作为防治肺炎支...     

miR-429对烧伤小鼠肺组织炎性反应和氧化应激的影响

目的 探讨miR-429对烧伤小鼠肺组织炎性反应和氧化应激的影响及可能的机制。方法 24只C57BL/6小鼠,按随机数表法分为对照组、模型组、阴性对照组和miR-429抑制剂组,每组6只。除对照组外,其他3组小鼠通过热水烫伤法构建小鼠烧伤模型。其中,miR-429抑制剂组和阴性对照组小鼠通过尾静脉分别注射等量的miR-429抑制剂miR-429 antagomir以及阴性对照miR-NC;对照组和模型组小鼠给予等体积0.9%氯化钠溶液。qRT-PCR实验检测肺组织中miR-429的表达水平;ELISA法检测肺组织中肿瘤坏死因子-α (TNF-α)、白介素-1β(IL-1β)、白细胞介素-6(IL-6)、丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH)水平;HE染色评估肺组织病理变化;TUNEL法检测肺组织细胞凋亡情况;Western blotting检测肺组织中Nrf2和HO-1蛋白表达情况。结果 与对照组小鼠比较,模型组小鼠肺泡壁变宽,并出现明显的组织水肿和炎症细胞浸润;肺组织中凋亡细胞数量明显增多,且miR-429表达、TNF-α、IL...     

布地奈德对哮喘大鼠碱性成纤维细胞生长因子蛋白和mRNA表达的影响

目的：观察碱性成纤维细胞生长因子在急性哮喘大鼠肺组织的表达情况及布地奈德的干预影响.方法：36只雄性SD大鼠随机分为对照组、哮喘组和布地纳德治疗组,以卵清白蛋白激发法制备哮喘模型,采用ELISA法测定支气管肺泡灌洗液中碱性成纤维细胞生长因子的含量,免疫组化和原位杂交法测定肺组织中碱性成纤维细胞生长因子蛋白和mRNA的表达情况.结果：支气管肺泡灌洗液中的碱性成纤维细胞生长因子浓度、肺组织碱性成纤维细胞生长因子蛋白和mRNA的表达水平哮喘组显著高于对照组（P＜0.01）,治疗组显著低于哮喘组（P＜0.01）,但与对照组相比仍较高（P＜0.01）,上皮细胞为主要表达细胞.结论：碱性成纤维细胞生长因子参与了哮喘的发病机制,布地奈德可抑制哮喘急性期碱性成纤维细胞生长因子蛋白和mRNA的表达增加效应,这可能是布地奈德抑制哮喘气道重塑的重要机制之一.     

长期雾化吸入4种非雾化剂型药物对健康SD大鼠肺组织的影响

目的:研究长期雾化吸入4种非雾化剂型药物对健康SD大鼠肺组织的损伤情况,评价其雾化吸入的安全性。方法:将40只健康SD大鼠(♂)按随机数字表法分为8组,分别为空白对照组、生理盐水组(溶剂对照)、布地奈德组(雾化剂型药物对照,0.1g/L)、二氧化硅组(肺损伤药物对照,40 g/L)和4种非雾化剂型药物组[定喘汤组(15 g/mL,以生药量计)、头孢曲松组(200 g/L)、清开灵组(原液)和痰热清组(原液)],每组5只。除空白对照组大鼠不作处理外,其余各组大鼠均雾化吸入给药,给药体积均为10mL,每天给药2次,连续给药56 d。给药结束后,对其外周血中白细胞进行分类、计数以及对支气管肺泡灌洗液中白细胞进行计数;苏木精-伊红染色观察其肺组织病理变化并进行尘细胞计数;免疫组化法检测其肺组织中白细胞分化抗原163(CD163)表达水平。结果:各组大鼠外周血中白细胞分类主要有淋巴细胞和中性粒细胞,其中又以淋巴细胞为主。与空白对照组比较,生理盐水组大鼠外周血中白细胞、淋巴细胞、中性粒细胞计数和肺泡灌洗液中白细胞计数以及肺组织中尘细胞计数差异均无统计学意义(P>0.05);支气管及肺组织结构完整,CD163表达为阴性。与生理盐水组比较,布地奈德组大鼠上述指标差异均无统计学意义(P>0.05),支气管及肺组织结构完整,CD163表达为阴性;而其余5组大鼠外周血中白细胞、淋巴细胞、中性粒细胞计数和支气管肺泡灌洗液中白细胞计数以及肺组织中尘细胞计数均显著升高(P<0.05);肺组织发生不同程度的肺泡壁增厚、肺泡间质水肿等病理变化,CD163表达均为阳性或强阳性。结论:4种非雾化剂型药物长期雾化吸入后可引起健康SD大鼠肺组织不同程度的病理改变,炎症细胞计数升高,肺泡中出现尘细胞。     

金茵清热口服液通过NF-κB/NLRP3信号通路改善小鼠急性肺损伤

目的 探究金茵清热口服液对脂多糖(LPS)诱导小鼠急性肺损伤的保护作用及机制。方法 C57BL/6J小鼠按随机数字表法分为6组：空白对照组、模型对照组、金茵清热口服液小剂量组、金茵清热口服液中剂量组、金茵清热口服液大剂量组和地塞米松组。除空白对照组,其他各组气管滴注LPS溶液(5 mg·kg^-1)构建小鼠急性肺损伤模型,金茵清热口服液低中高组连续灌胃给药3 d。24 h后,6组分别取小鼠肺组织和支气管肺泡灌洗液(bronchoalveolar larage fluid, BALF)进行后续检测,HE染色观察各组小鼠肺组织病理损伤;检测肺泡灌洗液总细胞数;BCA法检测BALF的总蛋白含量;ELISA法检测BALF中炎性细胞因子肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和免疫球蛋白M(IgM)的含量;免疫组化和Western blotting法检测肺组织核因子κB(NF-κB)、NOD样受体热蛋白结构域相关蛋白3(NLRP3)蛋白的表达情况。结果 与模型对照组比较,金茵清热口服液减轻了肺组织的病理学损伤(P<0.05...     

中药雾化治疗对慢阻肺大鼠气道炎症的研究

目的观察中药雾化吸入对慢性阻塞性肺疾病(COPD)大鼠模型肺炎性细胞及炎症介质IL-8、TNF-a含量变化的影响及意义,探讨其对COPD的防治机制。方法采用"烟熏复合木瓜蛋白酶雾化吸入法"复制COPD大鼠模型,随机分为治疗组、模型组、对照组。治疗组给予中药雾化吸入,模型组及对照组给予生理盐水雾化吸入,疗程为4周。观察肺泡灌洗液细胞学分类、血清IL-8及TNF-a含量、肺组织的病理变化。结果中药组肺泡灌洗液炎性细胞计数及血清炎性介质IL-8、TNF-a含量低于模型组(P<0.05);气管和支气管黏膜上皮脱落、气管软骨损毁、支气管腔内炎性细胞渗出等较模型组明显减轻。结论中药雾化能减轻支气管肺组织炎性细胞在肺内聚集,抑制炎性介质IL-8、TNF-a的产生,对COPD大鼠肺具有保护作用。     

玉簪花提取物对RAW264.7细胞炎症及哮喘小鼠气道炎症的影响

目的 研究玉簪花提取物对RAW264.7巨噬细胞炎症模型和BALB/c小鼠支气管哮喘模型的影响。方法 建立脂多糖与人干扰素-γ诱导的RAW264.7细胞炎症模型，用玉簪花提取物预处理模型细胞，测定细胞上清液中一氧化氮(NO)、白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)的水平。将BALB/c小鼠随机分为空白组、模型组、阳性组、玉簪花提取物高、低剂量组。采用卵清蛋白致敏和激发哮喘，末次给药24 h后，分析小鼠全血中淋巴细胞、单核细胞、粒细胞的数量，吉姆萨染色观察嗜酸性粒细胞的数目；ELISA法检测小鼠血清中总免疫球蛋白E(IgE)的水平、NO的含量、支气管肺泡灌洗液中IL-6与TNF-α的水平以及肺组织细胞黏附因子-1(ICAM-1)的水平；HE染色观察小鼠肺组织炎症及病理变化。结果 玉簪花提取物可显著抑制炎症细胞因子的表达；显著降低卵清蛋白模小鼠炎症细胞和嗜酸粒的数量，减少NO生成，降低IgE的含量，显著降低肺泡灌洗液中IL-6、TNF-α的水平以及肺组织中ICAM-1的表达。结论 玉簪花提取物对细胞炎症模型和哮喘气道炎症模型有较好的抑制作用，可为其治疗哮喘的研究提供参考。     

雾化吸入痰热清、喜炎平对大鼠肺部的刺激性研究

目的研究中药复方痰热清和单成分喜炎平注射液的雾化吸入对大鼠肺部的刺激性。方法每种药物分为高、低浓度2个实验组,对照组灌以生理盐水。雾化吸入药物给药7d后处死大鼠。采用大鼠支气管肺泡灌洗术,测定灌洗液中总蛋白含量和LDH酶活性,以判断两种药物对大鼠肺部的损伤程度。结果痰热清低、高浓度组肺泡灌洗液中蛋白质浓度分别为:(193.78±27.74)、(235.33±50.41)μg/ml;喜炎平两组蛋白质浓度为:(174.02±17.82)、(227.27±66.03)μg/ml;LDH酶活力单位依次为:1 065.21±181.76、1 467.33±101.87;307.97±47.56、1 377.29±566.48。经t检验,与对照组相比,痰热清和喜炎平(低浓度和高浓度)对肺泡灌洗液中总蛋白含量无显著影响,但均能增加LDH酶的活力(P<0.05),且与浓度呈正相关;低浓度痰热清组的LDH酶活力显著高于低浓度喜炎平组(P<0.05)。结论雾化吸入痰热清、喜炎平对大鼠呼吸系统有一定的刺激性,故不宜采用雾化吸入的给药方式。     

新生大鼠高氧性肺损伤肺组织内源性谷氨酸释放的变化

目的探讨谷氨酸在新生大鼠高氧性肺损伤中的作用。方法SD新生大鼠,出生后12h内随机分为空气对照组和高氧组。高氧组维持氧浓度≥95%,分别在1,3和7d后每组处死5只大鼠,取肺脏,测定肺组织湿重/干重(W/D)比值,HE染色观察肺组织病理变化;另取小鼠,进行支气管肺泡灌洗,制备支气管肺泡灌洗液(BALF),用血细胞计数板进行白细胞计数,全自动生化分析仪测定乳酸脱氢酶(LDH)活性,Lowry法检测总蛋白含量,高效液相色谱法检测谷氨酸含量。结果与空气对照组比较,持续高氧暴露1d新生大鼠肺组织W/D比值无明显变化,暴露3和7dW/D比值明显增加。HE染色可见,持续高氧暴露3d肺泡腔内少量炎症细胞渗出,暴露7d肺泡内红细胞和炎症细胞进一步增多,肺组织结构紊乱,肺泡数量减少。持续高氧暴露1d新生大鼠BALF中LDH活性明显增加,白细胞计数和总蛋白含量无明显变化,暴露3和7dBALF中LDH活性、总蛋白含量和白细胞计数均高于空气对照组。持续高氧暴露1和3dBALF中谷氨酸含量亦明显高于空气对照组。结论高浓度氧可引起新生大鼠急性肺损伤,诱导肺组织内源性谷氨酸的释放,提示谷氨酸在高氧性肺损伤中发挥重要作用。     

院内获得性肺炎患者支气管肺泡灌洗液病原菌分布及药敏结果分析

目的:了解支气管肺泡灌洗液(BALF)细菌培养及药敏试验在院内获得性肺炎(HAP)治疗中的应用价值。方法:对561例HAP患者BALF标本中的病原菌种类及药敏结果进行回顾性分析。结果:BALF培养阳性率46.9%,主要病原菌依次是白色念珠菌、鲍曼不动杆菌、铜绿假单胞菌、肺炎克雷伯菌。单一细菌感染占58.9%,混合细菌感染占41.1%。念珠菌对5-氟胞嘧啶、两性霉素B耐药率为0。产超广谱β-内酰胺酶(ESBLs)大肠埃希菌和肺炎克雷伯菌检出率分别为75.9%和35.7%,细菌多重耐药现象严重。结论:BALF细菌培养及药敏试验可为临床合理用药提供依据。     

Effect of blood leucocyte depletion on the inflammatory response of the lung to quartz

This study determined the effect of blood leucocyte depletion on the early inflammatory response of the lung to alpha-quartz. F344/N rats were instilled intratracheally with either physiological saline or 2 or 5 mg of alpha-quartz suspended in saline. One day prior to the instillation, half of the rats received an ip injection of rabbit antiserum that had been raised against rat neutrophils. The other half of the rats received an ip injection of normal rabbit serum. One day after the instillation of saline or quartz, the animals were euthanized and observed for changes in blood cell numbers, lung histopathology, and bronchoalveolar lavage fluid (BALF) content of indicators of an inflammatory response and cytotoxicity. The rabbit antiserum depleted the blood of most white blood cells of all types. BALF fluid from saline-instilled animals did not differ between the white blood cell-depleted and the nondepleted animals except for a 20% reduction in numbers of alveolar macrophages in the depleted animals. BALF fluid from the nondepleted, quartz-instilled animals had a dose-dependent increase in content of neutrophils and protein (indicator of an increase in the permeability of the alveolar/capillary barrier) as well as an increase in lactate dehydrogenase and glutathione reductase (cytoplasmic enzymes whose presence extracellularly indicates cytotoxicity), alkaline phosphatase (indicator of type II cell secretory activity), beta-glucuronidase, and acid proteinase (lysosomal enzymes) activities. The higher dose of quartz also elicited an increase in LTB4 and PGE2 content of BALF. GSH content of BALF was decreased by the quartz exposure. The depletion of blood white blood cells prevented the influx of neutrophils into the alveoli of the quartz-exposed rats and decreased the BALF markers of capillary permeability and cytotoxicity (protein content and extracellular cytoplasmic enzymes). The absence of neutrophils in the alveoli had no effect on the lysosomal content of BALF, indicating that the neutrophils were not the source of these enzymes in nondepleted rats exposed to alpha-quartz. The quartz-induced elevation of LTB4 in BALF was not observed in depleted rats, suggesting that neutrophils may be the source of the increase in this leukotriene in the BALF. Both the GSH content and the alkaline phosphatase activity in BALF were enhanced in the absence of alveolar neutrophils. The enhancement of GSH in BALF is consistent with the neutrophils being the source of reactive oxygen species that deplete GSH. The increased alkaline phosphatase activity in the BALF of both the depleted and nondepleted animals is consistent with the type II cell hypertrophy that was induced by quartz instillation and was neutrophil independent.(ABSTRACT TRUNCATED AT 400 WORDS)     

Dose-effect of inorganic tin on biochemical indices in rats

The dose-effect of stannous chloride on biochemical indices was examined in weanling male rats given oral doses of 0.3, 1.0 and 3.0 mg/kg at 12-h intervals for 90 days. The 3.0 mg/kg dose caused significant decreases of the relative weights of the femur, calcium concentration, lactic dehydrogenase and alkaline phosphatase activities in the serum, succinate dehydrogenase activity in the liver, and calcium content and acid phosphatase activity in the femoral diaphysis and epiphysis. Of the above indices, the 1.0 mg/kg dose produced significant reduction of succinate dehydrogenase activity in the liver, and calcium content and acid phosphatase activity in the femoral epiphysis. Those significant decreases were not observed with the 0.3 mg/kg dose, although a slight but not significant decrease of calcium content in the femoral epiphysis was observed. These results suggest that the no-effect level of inorganic tin orally administered would be lower than 0.6 mg/kg/day.     

Intratracheal instillation of zinc-cadmium sulfide (ZnCdS) in Fischer 344 rats

The purpose of this study was to assess the bioavailability and pulmonary toxicity of ZnCdS in rats. Groups of 30 male Fischer 344 rats each were anesthetized and dosed via intratracheal instillation with 5 mg of either ZnCdS, quartz (positive control), or titanium dioxide (TiO(2), negative control) suspended in 0.5 ml saline. A vehicle control group received 0.5 ml saline. Ten animals from each test group were sacrificed at 1 day, 1 wk, and 14 wk after dosing for bronchoalveolar lavage fluid (BALF) analysis and histopathology. The BALF was analyzed for alkaline phosphatase, acid phosphatase, lactate dehydrogenase (LDH), beta-glucuronidase (beta-glu), total protein, and cell counts. Two separate groups of 24 rats each were dosed as already described with either ZnCdS or saline. Eight rats from each group were sacrificed at 1 day, 1 wk, and 14 wk after dosing for determination of cadmium (Cd) and zinc (Zn) concentrations in the lung, liver, kidney, and blood. Results indicate that at 1 day after dosing, all enzyme activities (except acid phosphatase) and cell counts in BALF from the quartz and ZnCdS groups were significantly higher than in the TiO(2) and saline groups. At 7 days after dosing, high enzyme activity persisted in the quartz group, while the ZnCdS group showed only LDH and total protein levels significantly higher than the saline group. At 14 wk after dosing, LDH, total protein, beta-glu, and cell counts in the quartz group were significantly higher than all other groups. Histologic examination revealed interstitial inflammation and accumulation of foreign material in the lungs and mediastinal lymph nodes of quartz-, TiO(2)-, and ZnCdS-treated rats. Metal analyses in tissues showed profuse Cd and Zn concentrations in the lung 1 day after dosing, followed by a successive decline at 7 days and 14 wk after dosing. A very small, but statistically significant, amount of Cd and Zn was found in the kidneys at 14 wk after dosing. In conclusion, ZnCdS appears to cause temporary lung inflammation, is cleared slowly, and is poorly bioavailable.     

Adaptation to nephrotoxic effects of cephaloridine in subacute rat toxicity studies

The nephrotoxic effect of single iv daily doses of cephaloridine in rats for 10 to 15 days was investigated. Urine and serum samples and kidneys were analyzed 24 hr after the last injection. A circadian rhythm and dose-dependent increase of lactic dehydrogenase, alkaline phosphatase, and aminopeptidase occurred in the urine within the first 3 days. Nearly normal values were found after 10 days of application consistent but not correlating with a small degree of tubular injury as determined from the percentage of injured tubules in alkaline phosphatase-stained frozen sections. Measurements of the number of nucleated cells in the epithelium of proximal tubule cross sections and the number of tubular casts indicated an initial phase of cell degeneration and tubule necrosis followed by a phase of regeneration with young cells which tolerate larger doses of the nephrotoxic compound (up to twofold) than the original epithelium. This change of tubule cells was not reflected in the lactic dehydrogenase, aldolase, aminopeptidase, and/ or alkaline phosphatase content of the kidneys. Apparently the young cells in kidneys of rats injected daily released, as a nephrotoxic response, less lactic dehydrogenase into the urine than kidney cells 24 hr after a single dose.     

产超广谱β-内酰胺酶的大肠埃希菌和肺炎克雷伯菌所致医院感染的危险因素分析

目的:分析产超广谱β-内酰胺酶的大肠埃希菌和肺炎克雷伯菌(ESBLs-EK)所致医院感染的危险因素。方法:以2008-2010年产ESBLs-EK所致医院感染的84例患者为病例组,同期168例非产ESBLs-EK所致医院感染的患者为对照组,采用单因素和多因素Logistic回归分析其危险因素。结果:单因素分析表明,气管插管或切开,体内留置导管,含酶抑制剂、喹诺酮类、第3代头孢菌素类的应用是产ESBLs-EK所致医院感染的危险因素;多因素Logistic回归分析表明,气管插管或切开,含酶抑制剂、喹诺酮类及第3代头孢菌素类的应用是独立的危险因素。结论:ESBLs-EK所致医院感染的危险因素为多种,主要与抗菌药物如含酶抑制剂、喹诺酮类、第3代头孢菌素类的使用及侵袭性操作有关。     

Pulmonary surfactant as vehicle for intratracheally instilled tobramycin in mice infected with Klebsiella pneumoniae.

1. The use of pulmonary surfactant has been proposed as a vehicle for antibiotic delivery to the alveolar compartment of the lung. This study investigated survival rates of mice with a respiratory Klebsiella pneumoniae infection treated intratracheally with tobramycin using a natural exogenous surfactant preparation as vehicle. 2. At day 1 after infection, animals were injected intratracheally with 20 microliters of the following solutions: (1) a mixture of surfactant (500 micrograms) and tobramycin (250 micrograms); (2) tobramycin (250 micrograms) alone; (3) surfactant (500 micrograms) alone; and (4) NaHCO3 buffer (control, sham-treatment). A fifth group received no treatment (control). Deaths were registered every 12 h for 8 consecutive days. 3. The results show an increased survival in the group receiving the surfactant-tobramycin mixture compared to the group receiving tobramycin alone (P < 0.05), the group receiving surfactant alone (P < 0.01) and the control groups (P < 0.01). It is concluded that intratracheal instillation of surfactant-tobramycin is superior to tobramycin alone in protecting animals from death due to a respiratory Klebsiella pneumoniae infection.     

左氧氟沙星对肺炎克雷伯菌感染小鼠的治疗作用

目的:研究左氧氟沙星对实验性肺炎克雷伯菌感染小鼠的治疗作用。方法:鼻腔滴注法建立小鼠肺部肺炎克雷伯菌感染模型,给予不同剂量左氧氟沙星灌胃治疗,考察不同治疗组治疗过程中动物的死亡率、细菌浓度及最低抑菌浓度(MIC)变化情况。结果:15 mg·kg-1和90 mg·kg-1剂量组治疗前后MIC无明显变化;30 mg·kg-1主要选择低水平突变,MIC值较接种时升高2倍,而60 mg·kg-1剂量组则主要选择高水平突变,MIC值较接种时升高8倍。结论:不适宜剂量左氧氟沙星治疗肺炎克雷伯菌感染后会降低细菌敏感性,使MIC增加,诱导细菌逐渐耐药。     

Dopamine-beta-hydroxylase activity in serum of patients with hepatic damage.

1. The activity of dopamine-beta-hydroxylase (DBH) was assayed in the serum of 102 patients, mostly with varying degrees of hepatic dysfunction. 2. DBH activity was not elevated in those with liver disorder and did not correlate with serum bilirubin, transaminase, lactic dehydrogenase, alkaline phosphatase or creatine phosphokinase. 3. It is concluded that the liver is not necessarily involved in the inactivation of DBH.     

The effects of aflatoxin B1 on some testicular and kidney enzyme activity in rat

The effects of chronic intra-peritoneal administration of aflatoxin B₁ on the activity of alkaline and acid phosphatases; glutamic oxaloacetate (GOT) and pyruvaate transaminases (GPT); 5′-nucleotidase and lactic dehydrogenase enzymes were monitored in the testis and kidney opf adult albino rats. Results showed that aflatoxin B₁ depressed the activity of alkaline phosphatase in both tissues, but increased that of acid phosphatase in only the testis. While GOT and 5′-nucleotidase were inhibited, GPT and lactic dehydrogenase activity was enhanced by this carcinogen. These responses were similar for the testis and kidney.The above findings coupled with the microscopical observation of the testis tissue seem to indicate that the essential lesion of this toxin on the testis may be a modification of the enzymes of germinal cells resulting from a gradual depletion of the latter. Furthermore, the results appear to show that by and large, aflatoxin B₁ exerts only slightly different effects on the testis and kidney at the enzyme level.