An analysis of paul taylos working concepts

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An analysis of paul taylos working concepts

Figure 1 Immunohistochemical staining for glutathione S-transferase GST in the cerebellum of adult rat. A Weak staining with a-class GST antibody is present in the granule cell layer g and Purkinje cells arrow. No staining is observed in the molecular layer m. Control for nonspecific staining using preimmune serum.

Fixation of tissue with paraformaldehyde before immunohistochemical staining results in loss of immunoreactivity in the Purkinje cells. Figure 2 Immunohistochemical staining for class-specific GST in dorsal root ganglia of adult rat. A Antiserumagainst a-class GSTsstainsonly bar: B Staining ofneuronal cell bodies with p-GST antiserum.

C Intense stainingof dorsal root ganglia neurons and satellitecells with a-GST antiserum. Xenobiotic Metabolism in Bmin 25 Caution mustbe exercised ininterpretation of these findings for several reasons. First, the An analysis of paul taylos working concepts have been performed,in some cases, using antibodies that recognize subunits; in other cases, class-specificantibodies have been employed.

Furthermore, antibodies were always raised against hepatic GSTs, leavingopen the question of similarities and differences in immunoreactivity between brain and hepatic GSTs.

Procedures used for tissue fixation also influence immunoreactivity and, thus, interpretation of the apparent distribution of the GSTs see Fig.

Influences on Glutathione S-Tmnsferases in the Brain l Expression of the GST isozymes may be altered in response to xenobiotic exposure or pathophysiological state.

In many cases of xenobiotic-induced toxicity elevation of GST activity has been associated with decreased cellular or organ toxicity. Rat hepatic GST activity can be regulated at the transcriptional level by a variety of inducing agents, including the barbiturates e.

Furthermore, posttranslational modification of GST activity is suggested by reports of GST activation by active oxygen species Murataet al.

Little information is available on induction of specific classes of GST in the brain. Johnson and co-workers a noted increases in p-GST in some cerebellar Purkinje cells in hyperbilirubinemic Gunn rats. Administration of sulfadimethoxine, which displaces bilirubin from serum albumin, also increased levels of GST-4 in the flocculus and lateral regions, but not in the vermis of the cerebellum.

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Preliminary evidence from our laboratories suggest that there is class-specificinduction of GSTs in rat brain by phenobarbital and the neurotoxicant, monomeric acrylamide. The findings that the induction of GSTs is class-specific and that there arealso regional and gender differences ininduction in the brain make it probable that influences oninduction of GSTs in the brain will be similar to those known to influence their induction in liver i.

For example, rat liver contains preponderantly classes a and p GST, whereas the wisozyme is present in mouse liver Warholm et al. The mouse brain appears to possess activity than does the rat brain significantly greater total GST l-chloro-2,4-dinitrobenzene Das et al. The neurotoxicological significance of heterogeneities in the cellular distribution of constituents of the glutathione-conjugating systemare unknown.

The presenceof GSHand GSTs in the endothelia and astrocytes is consistent with these cells being the first line of defense between the blood vesseland theneuron.

In theabsence of GSTsto form excretable 16 Lowndes et al. The absence of significant levels of GSH in the neuron would suggestthat greater metabolic reliance is placed other on mechanisms of detoxification. Posttranslational methylation of the form of GST, which constitutes Under normal physiological conditions, GSH will inhibit the methylation of some proteins Neal et al.

A wide variety of neurotoxicants will alter tissue concentrations of GSH Meister,leaving open thepossibility of altered oxidation-reduction status in the cells as well as indirect actions on the capacity of the cells to carry out detoxification processes by the glutathione conjugating pathway.

Some examples likely reflectunique morphological or metabolic characteristics of the target cell, such as the involvement of cerebellar granule cells in methylmercury poisoning or myelin after hexachlorophene exposure.

Usually, thepattern of pathocliticinvolvement is not readily explained, and it may reflect still uncharacterized region- and cell-specific metabolism of xenobiotics to reactive or toxic intermediates. The following neurotoxic models illustrate remarkable cell specificity.

It is speculated that these pathoclitic responsesmay result from heterogeneous distribution of xenobiotic-metabolizing enzymes in the nervous system.

Phenytoin Phenytoin, widelyemployedin the treatment of seizure disorders, causes cerebellar symptoms suchas nystagmus, double vision, dysarthria, and ataxia following mild overdose, whereas suicidal intoxication has been noted to cause cerebellar atrophy Masur et al.

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Cerebellar Purkinje cells accumulatethe greatest quantities of radiolabeled phenytoin, but both Purkinje and granule cells appear tobe targets Savolainen et al. Purkinje cells in explanted mouse cerebellum are selectively vulnerable to phenytoin neurotoxicity Blank et al.

Long-term administration of phenytoin to mice or rats results in dystrophic changes in Purkinje cells, whereas granule cells show pyknosis. Additionally, swellings appear in Purkinje axons inthe deepcerebellar nuclei and in granule cell axom parallel fibers of the molecular layer Takeichi, ;Volk and Kirchgasser,; Volk et al.1 A Guide to the Microfilm Edition of The Garza Revolution, Records of the U.S.

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An analysis of paul taylos working concepts

E. The case study method in social inquiry. In: DENZIN, N. K. & LINCOLN, Yvonna S. The American tradition in qualitative research.

An analysis of paul taylos working concepts