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Neurotoxicity development

The cerebellar syndrome is the most common comph-cation of high-dose cytarabine therapy. In a study of the cerebellar syndrome caused by cytarabine (3), in which it was found in seven of 30 patients treated, symptoms of toxicity appeared between the third and seventh days of chemotherapy, manifesting first as lethargy and confusion (3). Within the next 24 hours there were signs of cerebellar dysfunction, including dysarthria, ataxia, tremor, nystagmus, and dysmetria. In most patients in whom neurotoxicity developed, liver function worsened during chemotherapy. Abnormal liver function at the start of therapy and the development of neurotoxicity appear to be linked. The symptoms of neurotoxicity resolved within 4-49 days. [Pg.1034]

Aschner M, Allen JW, Kimelberg HK, LoPachin RM, Streit WJ (1999) Glial cells in neurotoxicity development. Annu Rev Pharmacol Toxicol 39 151-173... [Pg.144]

The reason for the reduced susceptibility to capsaicin-induced degeneration of sensory neurons in the adult animal is not clear. If, however, the influx of calcium into ganglion cells is an indication of cell death, then it appears that in the rat resistance to neurotoxicity develops around the age of 10 days. After this time calcium was only occasionally detectable in sensory neurons (Jancso et aL, 1978). This is supported by more recent findings of Jancso and Kiraly (1981) who, using the Fink-Heimer technique, found degeneration in the dorsal horn of rats treated at 12 but not at 14 days of age. [Pg.195]

A particular mode of neurotoxicity was discovered for tricresyl phosphate that correlated with the presence of the o-cresyl isomer (or certain other specific aLkylphenyl isomers) in the triaryl phosphates. Many details of the chemistry and biochemistry of the toxic process have been elucidated (139,140,143—146). The use of low ortho-content cresols has become the accepted practice in industrial production of tricresyl phosphate. Standard in vivo tests, usually conducted with chickens sensitive to this mode of toxicity, have been developed for premarket testing of new or modified triaryl phosphates. As of 1992, the EPA called for extensive new toxicity and environmental data on this group of products (147). The Vederal e ster AoQ xm. ci. calling for this... [Pg.480]

Some polymyxins are sold for second-line systemic therapy. Polymyxin B sulfate and colistimethate sodium can be used for intravenous, intramuscular, or intrathecal administration, especially for Pseudomonas aerupinosa mP QXiosis, but also for most other gram-negative organisms, such as those resistant to first-line antibiotics. Nephrotoxicity and various neurotoxicities are common in parenteral, but not in topical, use. Resistance to polymyxins develops slowly, involves mutation and, at least in some bacteria, adaptation, a poorly understood type of resistance that is rapidly lost on transfer to a medium free of polymyxin. Resistance can involve changes in the proteins, the lipopolysaccharides, and lipids of the outer membrane of the cell (52). Polymyxin and colistin show complete cross-resistance. [Pg.149]

Clinical trials showed therapeutic efficacy in a broad spectrum of tumors these include SCLC, testicular tumors, sarcomas, breast cancer, renal cell cancer, pancreatic tumors and lymphomas. Ifosfamide is less myelosuppressive than cyclophosphamide but is more toxic to the bladder. Therefore it is recommended that ifosfamide is coadministered with the thiol compound mesna to avoid hemorrhagic cystitis and to reduce the risk of developing bladder cancer. Other side effects include neurotoxicity and myelosuppression. [Pg.55]

Hyjjerbilirubinaemia is an abnormality observed mainly in neonates in whom the liver is insufficiently developed to be able to detoxify the bile pigment bilirubin. This situation is known as neonatal jaundice and can sometimes become a serious disease causing neurotoxic symptoms. Bilirubin is produced by the degradation of heme [the Fe(II) complex of protoporphyrin IX] by heme oxygenase to give biliverdin, which is reduced by biliverdin reductase to... [Pg.429]

Pryor GT Persisting neurotoxic consequences of solvent abuse a developing animal modelfortoluene-inducedneurotoxicity. NlDAResMonogr 101 136—166,1990 Pudiak CM, Bozarth MA The effect of nitric oxide synthesis inhibition on intravenous cocaine self-administration. Prog Neuropsychopharmacol Biol Psychiatry 26 189— 196, 2002... [Pg.311]

The rapid growth in the use of OPs and the proliferation of new active ingredients and formulations was not without its problems. Some OPs proved to be too hazardous to operators because of very high acute toxicity. A few were found to cause delayed neurotoxicity, a condition not caused by ChE inhibition (e.g., mipafox, lepto-phos). There was also the problem of the development of resistance, for example, by... [Pg.193]

In the summary of the aforementioned report, the authors recommend, as did earlier reviewers of this subject, the development and evaluation of a tiered testing strategy for neurotoxicity. The further development of in vitro models for establishing mechanisms of neurotoxicity should be part of this strategy. Full consideration should also be given to advances in the omics and other technological fields. [Pg.315]


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