绵羊自然铅镉中毒骨骼损伤的X线特征

对自然铅镉中毒绵羊骨骼损伤的X线特征及骨组织重金属元素的沉积进行了系统研究。结果表明，由于重金属元素在骨骼中的高度蓄积，致使骨中Ca,P代谢紊乱，重金属中毒呈现以骨质疏松为特征的骨营养不良。头颅、胸部及四肢X线摄影检查显示，病羊骨骼主要病理变化是普遍性骨质疏松，牙齿磨灭不齐，四肢长骨密度减低，骨皮质变薄，骨髓腔增宽，骨小梁稀少，骨指数显著低于健康羊（P＜0．05）。     

Effect of Luteolin on Blood Indexes,Liver and Kidney in Mice with Acute Mercury Poisoning

To study the effect of luteolin on blood indexes,liver and kidney in mice with acute mercury poisoning,28 mice were randomly divided into four groups:Control group (intraperitoneal injection 0.9% saline),luteolin group (lavage 100 mg/kg luteolin),mercuric chloride group (intraperitoneal injection 4 mg/kg mercury chloride) and mercury chloride+luteolin group (intraperitoneal injection 4 mg/kg mercuric chloride,lavage 100 mg/kg luteolin).The activities of ALT in serum,AST,CREA and BUN contents,blood WBC,RBC,HGB content and GSH and MDA contents of liver tissue were detected.Morphological changes of liver and kidney tissues were observed.The results showed that compared with the control group,the activities of ALT and AST of mercuric chloride group were extremely significantly increased (P < 0.01),serum CREA,BUN,blood WBC and liver tissue MDA contents were significantly increased (P < 0.05) while blood RBC,HGB and liver tissue GSH contents were significantly decreased (P < 0.05).Liver,kidney pathological changes were obviously.Compared with mercuric chloride group,the activities of ALT,AST in serum,CREA,BUN,blood WBC and liver tissue MDA contents of mercuric chloride+luteolin group were significantly decreased (P < 0.05),while blood RBC,HGB and liver tissue GSH contents were significantly elevated (P < 0.05).Liver,kidney pathological changes were attenuated obviously.The poisoning were characterized by inflammation and the occurrence of anemia when acute mercury poisoning occurred,liver and kidney showed different degrees of injury in mice.Luteolin could reduce the toxic effects of acute mercury poisoning on blood,liver and kidney.     

1例藏獒三氮脒中毒的生化检验及治疗

用三氮脒以3.5 mg/kg的剂量对患有附红细胞体病的藏獒进行肌肉注射,隔日用同等剂量的三氮脒肌肉注射,24 h后,藏獒发生以神经症状为主的中毒现象,并表现出食欲废绝,后肢发软,四肢抽搐呈划水状,卧地不起,昏迷,体温正常临床症状。经血清生化检验,藏獒的尿素氮、肌酸激酶等的生化指标明显升高,血糖降低占病例的100%。经过5 d的药物治疗后,中毒藏獒基本恢复健康。     

叶酸对铅中毒幼年大鼠中枢神经系统的保护作用

通过研究铅对大鼠中枢神经元的损伤以及应用叶酸后的影响，探讨了叶酸对铅中毒条件下中枢神经元的保护作用。将健康清洁级初断乳3周龄SD大鼠随机分为铅染毒组，叶酸给药组及生理盐水组。各组于处理后第2、3、4周取材。铅染毒组、叶酸给药组每组各30只，生理盐水组12只，共72只。测量血铅，分别进行海马和小脑组织的H—E染色及凋亡抑制基因Bcl—2、凋亡基因Bax的蛋白免疫电泳，并作光密度分析。结果，通过对各个时间段各组血铅测定，可得叶酸给药组血铅含量低于铅染毒组。铅染毒组Bcl-2蛋白表达量少于给药组，而Bax多于给药组，H—E染色结果铅染毒组神经细胞数量明显少于叶酸给药组。结果表明，叶酸可降低铅中毒大鼠的血铅浓度，并具有一定抗细胞损伤作用，对铅中毒大鼠的中枢神经元具有一定的保护作用。     

食用醋精抑制亚硝酸盐产生的试验

亚硝酸盐中毒(Nitrite poisonig)是畜禽常发生的一种中毒病。用白菜等含硝酸盐较多的菜类作猪的饲料,因调制加工不合理,会产生大量的亚硝酸盐,喂后引起猪急性中毒,常来不急抢救而死亡,对养猪业危害较大。用食用醋精加入调制白菜的浸泡液中,使其pH值为4时,完全可抑制反硝化细菌的活动,基本上不会产生亚硝酸盐。这是因为醋酸是含有2个碳原子的有机酸,对反硝化细菌毒性大,使菌体内DNA和ATP受到破坏,细菌失去脱氮作用所致。用醋精作调制白菜的抑制剂,会起到预防畜禽亚硝盐中毒的作用。     

福建中、东部养殖贝类质量状况调查

2003～2005年对福建中、东部沿海的主要贝类养殖区养殖贝类进行质量抽检,品种包括菲律宾蛤仔、文蛤、牡蛎、贻贝及缢蛏,检测项目为汞、铅、砷、镉、石油烃等,并对检测结果进行分析讨论,结果表明大部分贝类产品卫生质量状况良好。     

Poisoning of horses by bamboo, Bambusa vulgaris

The clinical and pathological aspects of a neurological disease observed in 16 horses in Pará, Amazonia, Brazil, are presented. The symptoms were mainly motor incoordination, paresis of the tongue, somnolence, difficulties in apprehension, chewing and swallowing of food, as well as instability and standing with abducted members. The clinical course was subacute or chronic and in most cases was not fatal. Postmortem examination performed in one already very sick, euthanized animal, did not show significant macroscopic lesions; histopathological examination revealed slight edema and degenerative alterations of a few axons, mainly in the medulla oblongata. In all pastures where horses were affected, plenty of bamboo had been eaten, probably because of scarcity of pasture. By feeding large amounts of fresh bamboo leaves of this region, in different growing stages, to three horses (horse 1, 47 g/kg/d for 30 days; horse 2, 10 g/kg/d for 60 days; horse 3, 18 g/kg on the first day, and 31 g/kg/d for 6 more days)—the animals ate the leaves unassisted—it was possible to reproduce nervous symptoms essentially identical to those observed in the natural disease 24 to 72 hours after the first feeding of the plant. In spite of continuous administration of the plant, intensity of the clinical signs did not increase. Based on field observations and comparison of the clinical and pathological pictures seen in the natural and experimental disease, the described illness can be concluded to be caused by the ingestion of large amounts of the leaves of Bambusa vulgaris f. vulgaris.