Subcutaneous kerosene toxicity in albino rats

Biochemical, histopathological, and hematological parameters were studied in male Wistar rats after repeated subcutaneous administration of commercial kerosene (0.5 ml/kg body wt, 6 days a week) for a period of 35 days. At necropsy, treatment-related increases in the weights of liver, spleen, and peripheral lymph nodes were noted. Correspondingly, there was an increase in DNA, RNA, protein, and lipid contents of liver and spleen. Histopathological examination of liver, spleen, thymus, kidney, adrenal, and lymph nodes revealed treatment-related lesions. Similarly, biochemical indices studied in liver revealed an increase in alkaline phosphatase and a decrease in benzo[a]pyrene hydroxylase levels. Furthermore serum cholinesterase, carboxylesterase, and albumin levels were significantly diminished while serum alkaline phosphatase levels were found to be greatly enhanced. The findings might be related as the likely systemic effects in workers upon percutaneous kerosene exposure during work.     

Pathological changes in testes and liver of male albino rats after dermal exposure to DDVP insecticide.

Exposure of male albino rats to DDVP insecticide at sublethal dose of 30 mg/kg/day through dermal painting for a period of 90 days didn't show any intoxication symptoms or mortality. However, cytopathological changes in testicular and liver tissues were evident. There was a positive correlation between the degree of cellular damage and the period of insecticide administration. In general, damages were prominent in rats treated for 30 days or more. Histological examination of testes showed degenerative seminiferous tubules and fewer leydig cells. Hepatic cells were congested, atrophied and showed different stages of necrobiotic changes. This suggests a great care and caution for workers during different phases of DDVP insecticide handling.     

溴敌隆毒饵对大白鼠灭效和适口性观察

目的 测定溴敌隆毒饵对大白鼠的灭效和适口性。方法 无选择和有选择摄食试验。结果 毒杀率均为100％，死亡高峰在第6～8d，摄食系数0．63。结论 该毒饵杀灭效果和适口性好。     

Aphrodisiac and phytochemical studies of Cocculus hirsutus extracts in albino rats

ObjectiveTo investigate the in vivo aphrodisiac activity of various extracts obtained from aerial parts Cocculus hirsutus (C. hirsutus).MethodsWe evaluated whether oral administration of C. hirsutus has spermatogenic activity in male rats. Petroleum ether, chloroform and alcohol extract of aerial parts (stem and leaf) of C. hirsutus were administered at the dose level of 25 mg/100 g body weight to adult male albino rats for 30 days.ResultsThe above said extracts have stimulated the spermatogenic activity and accessory reproductive organs performance in albino rats. Out of the three extracts administered, alcohol extract showed highly stimulant spermatogenic effects in mature male albino rats. Alcohol extract showed potent androgenic activity when treated in immature Albino rats. Males treated with the extract displayed more frequent and vigorous anogenital sniffing and mounting as compared to untreated animals. The increased spermatogenesis in extract treated groups was confirmed by change in histoarchitecture as evidenced by increase in number of spermatogonia, spermatocyte, spermatids and caudal spermatozoa. After subjecting to preliminary phytochemical screening, the alcohol extract showed positive tests for steroids, saponins, oils and fats, phenolic compounds and tannins.ConclusionC. hirsutus exhibited remarkable increase in spermatogenic activity. These findings support the folk use of this plant as an aphrodisiac.     

脑纹状体多巴胺系统在急性CO中毒后的变化研究

目的观察急性一氧化碳(CO)中毒后纹状体多巴胺(DA)及其代谢产物含量的动态变化,探讨单胺氧化酶B(MAO-B)及DA系统变化在急性CO中毒迟发性脑病(delayed neruopsychologic sequelae,DNS)发病中的意义。方法采用腹腔注射CO法制备急性CO中毒大鼠模型,利用阿朴吗啡诱导旋转实验鉴定DNS模型,分析不同模型脑组织纹状体DA系统、MAO-B活性变化。结果急性CO中毒后纹状体MAO-B活性即明显降低,仅为对照组水平的43%;同时用清醒动物脑微透析实验观察纹状体DA及其代谢产物浓度变化发现,CO中毒后1 h DA浓度即增加,其代谢产物则明显降低,提示急性CO中毒早期DA代谢显著降低;中毒14 d后DNS模型大鼠纹状体MAO-B活性显著增加,为对照组活性的1.7倍,DA浓度则显著降低,仅为对照组的29%,代谢产物浓度明显增加,提示出现运动功能障碍的DNS模型脑纹状体MAO-B活性显著升高,DA代谢明显增加。结论急性CO中毒DNS大鼠脑纹状体MAO-B活性可异常升高,加速DA代谢,影响DA神经系统保持锥体及锥体外系运动协调功能,同时生成的大量DA代谢产物具有毒性作用,可进一步加重脑循环...     

Aspartame induced cardiac oxidative stress in Wistar albino rats

Aspartame (non-nutritive sweetener) is consumed by millions of people in products like beverages, instant breakfasts, desserts, breathe mints, sugar free chewing gum, vitamins, and pharmaceutical. On a weight basis, metabolism of aspartame generates approximately 50% phenylalanine, 40% aspartic acid and 10% methanol. The detailed mechanisms of their effects on cardiac tissue are still unclear. The present study aimed to clarify whether longer time aspartame consumption has any effect on heart of Wistar albino rats. Animals were randomly divided into 4 groups of 6 animals (group-1: control, group-2: folate deficient diet fed animals, group-3: control animals treated with aspartame, group-4: folate deficient diet fed animals treated with aspartame). Aspartame was given orally (40 mg/kg·bw/day), dissolved in normal saline and for 90 days. Since human beings have very low hepatic folate content, the folate deficient diet fed animals were used to mimic the human methanol metabolism. Aspartame consumption increased significantly plasma corticosterone level, suggesting that aspartame may act as a chemical stressor. There was a significant increase in lipid peroxidation, nitric oxide and protein carbonyl, and significant decrease in protein thiol, cardiac membrane bound ATPases (Na⁺, K⁺, Ca⁺⁺, Mg⁺⁺), enzymatic (SOD, CAT, GPX, G6PD, GR) and non-enzymatic antioxidants (GSH, Vit-C, Vit-E) as well as a significant increase in heart rate and heart marker enzymes (CK and CK-MB). It may be due to excessive generation of free radicals, which impairs cardiac function. Aspartame metabolite methanol or formaldehyde may be the causative factors behind these changes. However, up regulation of Hsp70 in immunohistochemical analysis of cardiac tissue might be a protective response to oxidative stress induced by aspartame metabolites and structural damages in cardiac tissue.     

锰对大鼠纹状体神经细胞凋亡的影响

目的利用锰染毒大鼠模型，分析不同浓度锰对大鼠纹状体神经细胞凋亡的影响，探讨锰神经毒性的作用机制。方法将健康雄性SD大鼠随机分成空白对照组和高、中、低3个剂量染锰组，每组6只动物。染毒结束，开颅分离取出大鼠纹状体，分别做锰含量测定、Tunel染色和透射电子显微镜观察。结果高、中、低3个剂量染锰组纹状体锰含量分别为（2．98±0．52）、（2．75±0．37）、（2．61±0．73）ng／mg，均高于空白对照组的（．60±0．20）ng／mg，差异有统计学意义（P〈0．05）。高、中、低3个剂量染锰组纹状体细胞凋亡指数分别为（24．83±5．98），（17．00±5．33），（15．33±2．58），均高于空白对照组的（2．83±0．41），差异有统计学意义（P〈0．05）。且随着染锰剂量的加大，细胞凋亡指数增加。染锰组大鼠纹状体的透射电子显微镜显示中剂量染锰时，部分纹状体神经细胞出现核变小、固缩，染色质浓集等细胞凋亡的特征性改变。结论锰可致大鼠纹状体神经细胞出现程度不同的细胞凋亡，而凋亡的程度与锰浓度有关。     

鱼藤酮染毒大鼠纹状体缝隙连接蛋白43的表达及意义

目的 观察鱼藤酮对大鼠中脑纹状体组织的毒性作用及对缝隙连接蛋白43(CX43)表达的影响. 方法 建立大鼠Alzet微泵恒流给药鱼藤酮染毒模型,应用光镜和免疫组织化学染色观察纹状体神经元和星形胶质细胞的形态改变,采用RT-PCR法检测CX43mRNA的表达,Western blot技术观察CX43蛋白活性变化.结果 染毒大鼠出现类帕金森病综合征特征,中脑纹状体组织神经元形态明显改变,星形胶质细胞增生.与正常对照组比较,2.0 mg/kg鱼藤酮染毒组CX43表达明显上调(P＜0.05),而4.0 mg/kg鱼藤酮染毒组CX43表达显著降低(P＜0.05). 结论 鱼藤酮可损伤中脑神经元,诱导大鼠出现类帕金森病症状,星形胶质细胞缝隙连接蛋白43的异常表达,可能参与了鱼藤酮对大鼠纹状体组织的毒性作用.