Hepatic UDP-glucuronyltransferase activity in acrylamide neuropathy.

Acrylamide was found to be tissue selective in its toxicity. Doses which were clearly neurotoxic to rats were without effect on hepatic UDP-glucuronyltransferase, total hepatic protein or microsomal protein.     

Hepatic drug metabolizing activity in lead-poisoned rats

Zusammenfassung Eine Verminderung der Konzentration von Cytochrom P-450 sowie der Aktivität von arzneimittelabbauenden Enzymen tritt in der Rattenleber nach Bleivergiftung auf. Intensität und Dauer sind dosisabhängig (10–100 mol Pb(NO₃)₂ pro kg Körpergewicht).

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Publication No. 883 of Directorate for biology (D.G. III) —European Communities Commission.     

Impairment of rapid axonal transport and concomitant anomaly of smooth endoplasmic reticulum in acrylamide induced neuropathy]

The axonal transport of proteins was studied by radioautography in preganglionic axons of ciliary ganglia in Leghorn chickens treated by acrylamide. The slow axonal transport of proteins was hardly affected. In contrast, the fast axonal transport was severely impaired. Indeed, radioactive proteins accumulated focally at the periphery of several preterminal axons in regions showing a local disorganization of the smooth endoplasmic reticulum which seemed to be one of the earliest changes induced by acrylamide.     

The effect of imipramine and desipramine on UDP-glucuronyltransferase

Zusammenfassung Der Einfluss von Imipramin und Desipramin auf die Umwandlung von Bilirubin undo-Aminophenol in deren jeweilige Glukuronide wurde in vitro in der Leber untersucht. Imipramin blockiert die Umwandlung von Bilirubin und vono-Aminophenol, während Desipramin nur diejenige vono-Aminophenol blockiert.     

Giant axonal neuropathy

Giant axonal neuropathy (GAN) is a rare autosomal recessive disorder affecting both the central and peripheral nervous systems. Cytopathologically, the disorder is characterized by giant axons with derangements of cytoskeletal components. Geneticists refined the chromosomal interval containing the locus, culminating in the cloning of the defective gene, GAN. To date, many distinct mutations scattered throughout the coding region of the locus have been reported by researchers from different groups around the world. GAN encodes the protein, gigaxonin. Recently, a genetic mouse model of the disease was generated by targeted disruption of the locus. Over the years, the molecular mechanisms underlying GAN have attracted much interest. Studies have revealed that gigaxonin appears to play an important role in cytoskeletal functions and dynamics by directing ubiquitin-mediated degradations of cytoskeletal proteins. Aberrant accumulations of cytoskeletal-associated proteins caused by a defect in the ubiquitinproteasome system (UPS) have been shown to be responsible for neurodegeneration occurring in GAN-null neurons, providing strong support for the notion that UPS plays crucial roles in cytoskeletal functions and dynamics. However, many key questions about the disease remain unanswered. Received 6 September 2006; received after revision 11 October 2006; accepted 5 December 2006 Y. Yang, E. Allen The authors contributed equally to this work.     

Hepatic protein turnover in goldthioglucose-induced obesity

Summary Goldthioglucose obese mice fail to regulate hepatic protein turnover in response to variable energy intake in contrast to lean mice.     

50 ppm MnBK subclinical neuropathy in rats

Summary 40 rats were subjected daily for 6 months to an atmosphere containing 50 ppm MnBK. 32 of the rats presented with demyelination of the sciatic nerve and 2 of these with axonal hypertrophy.This work was supported in part by General Support Grant RR. 5414.We thank Dr Cedric Raines, Einstein Medical Center, New York, for helpful criticisms and suggestions and Dr Saul Francis for intoxicating the rats.     

Electrophoresis of mitochondrialα-l-glycerophosphate dehydrogenase on acrylamide gels

Zusammenfassung Es wird ein Verfahren zur elektrophoretischen Trennung am Polyacrylamid der an die Mitochondrien gebundene -L-Glyzeraldehydphosphat-Dehydrogenase in 2 aktive Bestandteile beschrieben: Partielle Spaltung der Eiweissmolekeln mit Harnstoff. Die Auflösung der Enzyme in 2 aktive Komponenten wurde mit Extrakten aus Mitochondrien verschiedener Rattenorgane (Leber, Niere, Hirn, Hoden und Hepatoma 5123 A) sowie Mäuseleber verfolgt.     

Ultracentrifugation of yeast cells in a gradient of acrylamide gel and sucrose

Zusammenfassung Dichtegefälle-Ultrazentrifugation, verbunden mit Photopolymerisation von Akrylamid, ist geeignet um lebende, unverletzte Zellen unbeweglich in Bänder zu trennen, insofern sie sich punkto Gewicht, Volumen, Dichte oder Beweglichkeit im Dichtegefälle unterscheiden. Verschieden ernährte Hefezellen-Gruppen (Candida albicans) zeigten verschiedene Bandenverteilungen.     

50ppm MnBK subclinical neuropathy in rats.

40 rats were subjected daily for 6 months to an atmosphere containing 50ppm MnBK. 32 of the rats presented with demyelination of the sciatic nerve and 2 of these with axonal hypertrophy.     

Hepatic blood flow in acute myocardial ischemia

Summary Hepatic blood flow was monitored in cats during myocardial ischemia (MI). Increased plasma CPK activity, the S-T segment of the electrocardiogram, and hepatic flow was reduced by 5 h to 40% of control. The results suggest that MI can influence organs distant from the original ischemic episode.Supported in part by Research grant HL-17745 from the National Heart, Lung and Blood Institute of the National Institutes of Health.Acknowledgments. We gratefully acknowledge the expert technical assistance of Mary Ann Spath.     

Hepatic blood flow in acute myocardial ischemia

Hepatic blood flow was monitored in cats during myocardial ischemia (MI). Increased plasma CPK activity, the S-T segment of the electrocardiogram, and hepatic flow was reduced by 5 h to 40% of control. The results suggest that MI can influence organs distant from the original ischemic episode.     

Two-dimensional electrophoresis of rat serum esterases in cellulose acetate and acrylamide gradient gel

Zusammenfassung Isoenzyme von Serumesterasen wurden zuerst mit Zelluloseazetat und dann mit einem Gradientgel von Polyakrylamid mit zweidimensionaler Elektrophorese bei der Ratte untersucht. Ein neues Band, das eine starke Albuminesteraseaktivität aufweist und unempfindlich gegen 10^–3 M Physostigmin ist, wurde somit gefunden. Von 17 Esterasebändern waren 7 empfindlich auf Physostigmin, und 3 wurden auch durch Iso-OMPA gehemmt, während 284-C-51 gar keinen Effekt zeigte.

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Supported by a grant from the Sigrid Jusélius Foundation, Finland.     

Testosterone derivatives are neuroprotective agents in experimental diabetic neuropathy

In this study we have assessed the effect of testosterone (T), dihydrotestosterone (DHT) and 5αandrostan-3α, 17β-diol (3α-diol) therapies on diabetic neuropathy. Diabetes was induced in adult male rats by the injection of streptozotocin and resulted in decreased T and increased 3α-diol levels in plasma and in decreased levels of pregnenolone and DHT in the sciatic nerve. Moreover, a reduced expression of the enzyme converting Tinto DHT (i.e., the 5α-reductase) also occurs at the level of sciatic nerve, suggesting that the decrease of DHT levels could be due to an impairment of this enzyme. Chronic treatment for 1 month with DHT or 3α-diol increased tail nerve conduction velocity and partially counteracted the increase of thermal threshold induced by diabetes. Treatment with DHT increased tibial Na⁺,K⁺-ATPase activity and the expression of myelin protein P0 in the sciatic nerve.DHT, 3α-diol and T reversed the reduction of intra-epidermal nerve fiber density induced by diabetes. These observations indicate that T metabolites can reverse behavioral, neurophysiological, morphological and biochemical alterations induced by peripheral diabetic neuropathy. I. Roglio, R. Bianchi: These authors contributed equally to this study. Received 4 January 2007; received after revision 13 February 2007; accepted 27 March 2007