Info on Glutathione

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> From: Holly Moore
> To: [log in to unmask]
> Subject: glutathione stuff
> Date: Thursday, March 20, 1997 10:01 AM
>
> Hi Jim
>
> Here are some references related to glutathione.  I'll grab them at
> the library. I'll make copies for you.
>
> Holly
>
>
> <1>
> Unique Identifier
>   97041179
> Authors
>   Raha A.  Tew KD.
> Institution
>   Department of Pharmacology, Fox Chase Cancer Center, Philadelphia, PA
19111,
>   USA.
> Title
>   Glutathione S-transferases. [Review] [363 refs]
> Source
>   Cancer Treatment & Research.  87:83-122, 1996.
>
> <2>
> Unique Identifier
>   96386474
> Authors
>   Dekant W.
> Institution
>   Institut fur Toxikologie und Pharmakologie, Universitat Wurzburg,
Germany.
> Title
>   Biosynthesis and cellular effects of toxic glutathione
>   S-conjugates. [Review] [115 refs]
> Source
>   Advances in Experimental Medicine & Biology.  387:297-312, 1996.
>
> <3>
> Unique Identifier
>   97119162
> Authors
>   Jenner P.  Olanow CW.
> Institution
>   Neurodegenerative Diseases Research Centre, King's College London, UK.
> Title
>   Oxidative stress and the pathogenesis of Parkinson's disease. [Review]
[128
>   refs]
> Source
>   Neurology.  47(6 Suppl 3):S161-70, 1996 Dec.
> Abstract
>   Current concepts of the pathogenesis of Parkinson's disease (PD) center
on
>   the formation of reactive oxygen species and the onset of oxidative
stress
>   leading to oxidative damage to substantia nigra pars compacta.
Extensive
>   postmortem studies have provided evidence to support the involvement of
>   oxidative stress in the pathogenesis of PD; in particular, these
include
>   alterations in brain iron content, impaired mitochondrial function,
>   alterations in the antioxidant protective systems (most notably
superoxide
>   dismutase [SOD] and reduced glutathione [GSH]), and evidence
>   of oxidative damage to lipids, proteins, and DNA. Iron can
>   induce oxidative stress, and intranigral injections have been shown to
induce
>   a model of progressive parkinsonism. A loss of GSH is associated with
>   incidental Lewy body disease and may represent the earliest biochemical
>   marker of nigral cell loss. GSH depletion alone may not result in
damage to
>   nigral neurons but may increase susceptibility to subsequent toxic or
free
>   radical exposure. The nature of the free radical species responsible
for cell
>   death in PD remains unknown, but there is vidence of involvement of
hydroxyl
>   radical (OH.), peroxynitrite, and nitric oxide. Indeed, OH. and
peroxynitrite
>   formation may be critically dependent on nitric oxide formation.
Central to
>   many of the processes involved in oxidative stress and oxidative damage
in PD
>   are the actions of monoamine oxidase-B (MAO-B). MAO-B is essential for
the
>   activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to
>   1-methyl-4-phenylpyridinium ion, for a component of the enzymatic
conversion
>   of dopamine to hydrogen peroxide (H2O2), and for the activation of
other
>   potential toxins such as isoquinolines and beta-carbolines. Thus, the
>   inhibition of MAO-B by drugs such as selegiline may protect against
>   activation of some toxins and free radicals formed from the MAO-B
oxidation
>   of dopamine. In addition, selegiline may act through a mechanism
unrelated to
>   MAO-B to increase neurotrophic factor activity and upregulate molecules
such
>   as glutathione, SOD, catalase, and BCL-2
>   protein, which protect against oxidant stress and apoptosis.
>   Consequently, selegiline may be advantageous in the long-term treatment
of
>   PD. [References: 128]
>
> <4>
> Unique Identifier
>   97064389
> Authors
>   Bauer AJ.
> Institution
>   Department of Medicine/Gastroenterology, University of Pittsburgh
Medical
>   Center, PA 15261, USA.
> Title
>   Transplantation-induced injuries of the intestinal muscularis and its
>   innervation: from preservation to chronic rejection. [Review] [11 refs]
> Source
>   Transplantation Proceedings.  28(5):2539-41, 1996 Oct.
>
> <5>
> Unique Identifier
>   96400488
> Authors
>   Smith CV.  Jones DP.  Guenthner TM.  Lash LH.  Lauterburg BH.
> Institution
>   Department of Pediatrics, Baylor College of Medicine, Houston 77030,
USA.
> Title
>   Compartmentation of glutathione: implications for the study
>   of toxicity and disease. [Review] [82 refs]
> Source
>   Toxicology & Applied Pharmacology.  140(1):1-12, 1996 Sep.
> Abstract
>   The fact that glutathione (GSH) plays many roles in
>   biological protective mechanisms and critical physiological
functionshas
>   been recognized for decades. Conjugates, disulfides, and
>   other glutathione-derived products also have been studied as
>   biomarkers of the chemical natures or specific identities of key
metabolites
>   of toxic agents and such studies have been crucial in the delineation
of the
>   nature of the interactions of proximal toxicants with target
biomolecules.
>   Despite the extensive evidence implicating the depletion and/or
oxidation of
>   glutathione in a wide variety of human and experimental
>   toxicities, critical examination of such studies frequently reveals
that
>   injury is not simply related to glutathione status. GSH is
>   compartmentalized at several levels and this compartmentation appears
to
>   exert considerable influence on the relationships between
>   glutathione depletion or oxidation and the onset of injury.
>   Although compartmentation is usually viewed from the perspective of
different
>   intracellular pools, the significance of extracellular
>   glutathione in functionally important pools is gaining
>   recognition. As the factors affecting the interactions of intracellular
pools
>   with extracellular pools are delineated, studies in humans can be
designed
>   and interpreted with greater precision and utility. [References: 82]
>
> <6>
> Unique Identifier
>   96318992
> Authors
>   Jenner P.
> Institution
>   Biomedical Sciences Division, King's College London, UK.
> Title
>   Oxidative stress in Parkinson's disease and other neurodegenerative
>   disorders. [Review] [51 refs]
> Source
>   Pathologie Biologie.  44(1):57-64, 1996 Jan.
> Abstract
>   The cause of cell death in neurodegenerative diseases remains unknown
but the
>   formation of free radicals and the occurrence of oxidative stress may
be a
>   common component of many, if not all, such disorders. For example, in
>   substantia nigra in Parkinson's diseases key alterations occur, in iron
>   handling, mitochondrial function and antioxidant defences, particularly
>   reduced glutathione. These indices of oxidative stress are
>   accompanied by evidence of free radical mediated damage inthe form of
>   increased lipid peroxidation and oxidation of DNA bases. The
alterations in
>   oxidative stress occurring in Parkinson's disease appear not be related
to
>   the administration of L-DOPA. Some alterations of oxidative stress are
found
>   in other basal ganglia in degenerative disorders (multiple system
atrophy,
>   progressive supranuclear palsy, Huntington's disease) but these have
not been
>   investigated to the same extent. Similarly, examination of biochemical
>   changes occurring in Alzheimer's disease, motor neurone disease and
diabetic
>   neuropathy also suggest the involvement of free radical mediated
mechanisms
>   as a component of neurodegeneration. It is probable that irrespective
of the
>   primary cause of individual neurodegenerative disorder, the onset of
>   oxidative stress is a common mechanism by which neuronal death occurs
and
>   which contributes to disease progression. Clearly, therapeutic
strategies
>   aimed at limiting free radical production and oxidative stress and/or
damage
>   may slow the advance of neurodegenerative disease. [References: 51]
>
> <7>
> Unique Identifier
>   96260934
> Authors
>   Ebadi M.  Srinivasan SK.  Baxi MD.
> Institution
>   Department of Pharmacology, University of Nebraska College of Medicine,
Omaha
>   68198-6260, USA.
> Title
>   Oxidative stress and antioxidant therapy in Parkinson's disease.
[Review]
>   [340 refs]
> Source
>   Progress in Neurobiology.  48(1):1-19, 1996 Jan.
> Abstract
>   Parkinson's disease, known also as striatal dopamine deficiency
syndrome, is
>   a degenerative disorder of the central nervous system characterized by
>   akinesia, muscular rigidity, tremor at rest, and postural
abnormalities. In
>   early stages of parkinsonism, there appears to be a compensatory
increase in
>   the number of dopamine receptors to accommodate the initial loss of
dopamine
>   neurons. As the disease progresses, the number of dopamine receptors
>   decreases, apparently due to the concomitant degeneration of dopamine
target
>   sites on striatal neurons. The loss of dopaminergic neurons in
Parkinso's
>   disease results in enhanced metabolism of dopamine, augmenting the
formation
>   of H2O2, thus leading to generation of highly neurotoxic hydroxyl
radicals
>   (OH.). The generation of free radicals can also be produced by
>   6-hydroxydopamine or MPTP which destroys striatal dopaminergic neurons
>   causing parkinsonism in experimental animals as well as human beings.
Studies
>   of the substantia nigra after death in Parkinson's disease have
suggested the
>   presence of oxidative stress and depletion of reduced
>   glutathione; a high level of total iron with reduced level
>   of ferritin; and deficiency of mitochondrial complex I. New approaches
>   designed to attenuate the effects of oxidative stress and to provide
>   neuroprotection of striatal dopaminergic neurons in Parkinson's disease
>   include blocking dopamine transporter by mazindol, blocking NMDA
receptors by
>   dizocilpine maleate, enhancing the survival of neurons by giving
>   brain-derived neurotrophic factors, providing antioxidants such as
vitamin E,
>   or inhibiting monoamine oxidase B (MAO-B) by selegiline. Among all of
these
>   experimental therapeutic refinements, the use of selegiline has been
most
>   successful in that it has been shown that selegiline may have a
neurotrophic
>   factor-like action rescuing striatal neurons and prolonging the
survival of
>   patients with Parkinson's disease. [References: 340]
>
> <8>
> Unique Identifier
>   96296549
> Authors
>   O'Brien ML.  Tew KD.
> Institution
>   Department of Pharmacology, University of Pennsylvania, Philadelphia
19111,
>   USA.
> Title
>   Glutathione and related enzymes in multidrug resistance.
>   [Review] [147 refs]
> Source
>   European Journal of Cancer.  32A(6):967-78, 1996 Jun.
>
> <9>
> Unique Identifier
>   96279694
> Authors
>   Duggin GG.
> Institution
>   Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney,
>   Australia.
> Title
>   Combination analgesic-induced kidney disease: the Australian
experience.
>   [Review] [41 refs]
> Source
>   American Journal of Kidney Diseases.  28(1 Suppl 1):S39-47, 1996 Jul.
> Abstract
>   Analgesi nephropathy is a unique drug-induced kidney disease
characterized
>   pathologically by renal papillary necrosis and chronic interstitial
>   nephritis, and is the result of excessive consumption of combination
>   antipyretic analgesics. The clinical features of the disorder relate
mainly
>   to the papillary necrosis, renal colic, and obstructive uropathy and
the
>   development of chronic renal failure in a small percentage of patients.
There
>   are significant geographic variations in the clinical features that may
be
>   related to the differing combinations of analgesics. The pathogenesis
of the
>   disease is in part related to the kidneys' ability to concentrate drugs
in
>   the papillae. The following sequence of events presents a plausible
>   explanation for the evolution of the disease. If a combination of
phenacetin
>   and aspirin is ingested, the following steps occur. Phenacetin is
converted
>   in the gut and liver to acetaminophen by first-pass metabolism.
Acetaminophen
>   is then taken up by the kidney and excreted. During its excretion,
>   acetaminophen becomes concentrated in the papillae of the kidney during
>   physiologic degrees of antidiuresis, the concentration being up to five
times
>   the intracellular concentration of other tissues. Acetaminophen
undergoes
>   oxidative metabolism by prostaglandin H synthase to a reactive
quinoneimine
>   that is conjugated to glutathione. If acetaminophen is
>   present alone, there is sufficient glutathione generated in
>   the papillae to detoxify the reactive intermediate. If the
acetaminophen is
>   ingested with aspirin, the aspirin is converted to salicylate and
salicylate
>   becomes highly concentrated in both the cortex and papillae of the
kidney.
>   Salicylate is a potent depletor of glutathione. The
>   mechanism is not completely understood; however, the inhibition of the
>   production of NADPH via the pentose shunt is a possible explanation.
With the
>   cellular glutathione depleted, the reactive metabolite of
>   acetaminophen then produces lipid peroxides and arylation of tissue
proteins, ultimately resulting in necrosis of the papillae.
>   [References: 41]
>
> <10>
> Unique Identifier
>   96218587
> Authors
>   Taylor CG.  Nagy LE.  Bray TM.
> Institution
>   Department of Foods and Nutrition, University of Manitoba, Winnipeg,
Canada.
> Title
>   Nutritional and hormonal regulation of glutathione
>   homeostasis. [Review] [129 refs]
> Source
>   Current Topics in Cellular Regulation.  34:189-208, 1996.
>
> <11>
> Unique Identifier
>   96094704
> Authors
>   Meydani SN.  Wu D.  Santos MS.  Hayek MG.
> Institution
>   Nutritional Immunology Laboratory, Jean Mayer US Department of
Agriculture
>   Human Nutrition Research Center on Aging, Tufts University, Boston, MA
02111,
>   USA.
> Title
>   Antioxidants and immune response in aged persons: overview of present
>   evidence. [Review] [146 refs]
> Source
>   American Journal of Clinical Nutrition.  62(6 Suppl):1462S-1476S, 1995
Dec.
> Abstract
>   The oxidant-antioxidant balance is an important determinant of immune
cell
>   function, including maintaining the integrity and functionality of
membrane
>   lipids, cellular proteins, and nucleic acids and controlling
>   signal transduction and gene expression in immune cells. Optimal
amounts of
>   antioxidants are needed for maintenance of the immune response across
all age
>   groups. This need might be more critical, however, in aged persons.
>   Age-associated dysregulation of immune response, particularly of T
>   cell-mediated function, is well documented. The well-known age-related
>   increase in free radical formation and lipid peroxidation contributes,
at
>   least in part, to this phenomenon. We summarize animal and human
studies
>   undertaken by ourselves as well as other investigators on the effects
of
>   antioxidants, vitamin E, beta-carotene, and glutathione on
>   the immune response of aged persons. The underlying mechanisms for the
>   antioxidant nutrients' effects as well as their health implications for
aged
>   persons are discussed. [References: 146]
>
> <12>
> Unique Identifier
>   96275338
> Authors
>   Schulz JB.  Matthews RT.  Beal MF.
> Institution
>   Neurochmistry Laboratory, Massachusetts General Hospital, Boston, USA.
> Title
>   Role of nitric oxide in neurodegenerative diseases. [Review] [42 refs]
> Source
>   Current Opinion in Neurology.  8(6):480-6, 1995 Dec.
> Abstract
>   Besides its role as a mediator of several physiological functions,
nitric
>   oxide appears to be a neurotoxin under conditions of excessive
production,
>   which suggests a role for nitric oxide in neurodegenerative diseases.
An
>   increasing body of evidence has implicated excitotoxicity as a
mechanism of
>   cell death in both acute and chronic neurologic diseases. Activation of
>   excitatory amino acid receptors leads to activation of neuronal nitric
oxide
>   synthase by an increase in intracellular calcium concentrations. Nitric
oxide
>   may inhibit key enzymes of energy metabolism, damage DNA, deplete
>   intracellular glutathione, and react with superoxide to form
>   peroxynitrite. The latter is a highly reactive molecule, a potent
oxidizing
>   agent known to initiate lipid peroxidation, hydroxylation and nitration
of
>   aromatic amino acid residues, and sulfhydryl oxidation of
>   proteins, and to decompose to nitrogen dioxide and species
>   with hydroxyl-like reactivity. There now is evidence that the neuronal
>   production of nitric oxide and the formation of peroxynitrite occurs in
vivo.
>   [References: 42]