Inhibition of hormone-stimulated ornithine decarboxylase activity by lithium chloride

Richards, Jennifer H.; Fox, Kelly; Peng, Ted; Hsiao, Jerry; Gout, Peter W.

doi:10.1016/0024-3205(90)90325-l

Cited by 10 publications

(8 citation statements)

References 26 publications

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“…As a possible mechanism for this effect, they show that LiCl-pretreated progenitors change their membrane levels of receptors for cytokines pivotal for their expansion and differentiation, such as Flt3L. Lithium's role on functional thymocytes study 70 showed that chronic treatment with LiCl produced significant involution of the thymus gland and it is not mediated by adrenocortical mechanisms or stress. While on hormone-based study effects 71 of LiCl on hormonestimulated ornithine decarboxylase (ODC) activity were determined in kidney and liver of rats treated with dexamethasone or prolactin (PRL) and also in cultured, PRLstimulated Nb2 lymphoma cells.…”

Section: Lithium Effects On Thymocytesmentioning

confidence: 96%

Review of lithium effects on immune cells

Maddu¹,

Raghavendra²

2015

Immunopharmacology and Immunotoxicology

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One of the remarkable discoveries in the field of psychopharmacology from late 1940s is Lithium (Li) that reminds of old but still gold. It continues to be a distinctive mood stabilizer that matches various standards recommended for mood stabilizers. Apart from this Li is also known to affect immune cell functions. Lithium response and regulations of different immune cells in bipolar patients, related immune disorders are not well defined. Here, we provide an overview of literature with regard to Li's effects on different immune cells. However, the use of Li is currently limited to bipolar disorders and there is no empirical evidence for immune cell disorders. The objective of this article is to provide the evaluations of Li responses towards the different immune cells based on the existing studies. Further, more studies are needed to understand the mechanistic basis and heterogeneous responses of Li's effect in bipolar, also unravel relative immune disorders.

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Section: Lithium Effects On Thymocytesmentioning

confidence: 96%

Review of lithium effects on immune cells

Maddu¹,

Raghavendra²

2015

Immunopharmacology and Immunotoxicology

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“…The rate-limiting steps of polyamine biosynthesis are the formation of putrescine, the diamine precursor, catalyzed by ornithine decarboxylase (ODC; L-ornithine carboxy-lyase; EC 4.1.1.17), and the formation of decarboxylated S-adenosylmethionine (SAM), catalyzed by SAM decarboxylase (SAMDC; SAM carboxy-lyase; EC 4.1.1.50). These two regulatory enzymes of polyamine biosynthesis have short biological half-lives (10-20 mm) and are inducible by various physiological (hormones and growth factors) and pathological (brain injury, neurotoxin and ischemic insult, seizure activity, and hypoosmotic stress) stimuli (Pajunen et a!., 1978;Dienel and Cruz, 1984;Au et al, 1987;Paschen et a!., 1988;Reed and de Belleroche, 1989;Richards et al, 1990;Porcella et al, 1991;Crozat et a!., 1992;Hayashi et a!., 1992). The activity of ODC is also regulated by polyamine levels, which can affect the stability of the enzyme and alter the translation rate of ODC mRNA, with decreased levels eliciting enhanced translation and elevated levels causing decreased translation.…”

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confidence: 99%

Ornithine Decarboxylase in Human Brain: Influence of Aging, Regional Distribution, and Alzheimer's Disease

Morrison

Cao

Kish

1998

Journal of Neurochemistry

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Although experimental animal data have implicated ornithine decarboxylase, a key regulatory enzyme of polyamine biosynthesis, in brain development and function, little information is available on this enzyme in normal or abnormal human brain. We examined the influence, in autopsied human brain, of postnatal development and aging, regional distribution, and Alzheimer's disease on the activity of ornithine decarboxylase. Consistent with animal data, human brain ornithine decarboxylase activity was highest in the perinatal period, declining sharply (by '-60%) during the first year of life to values that remained generally unchanged up to senescence. In adult brain, a moderately heterogeneous regional distribution of enzyme activity was observed, with high levels in the thalamus and occipital cortex and low levels in cerebellar cortex and putamen. In the Alzheimer's disease group, mean ornithine decarboxylase activity was significantly increased in the temporal cortex (+76%), reduced in occipital cortex(-70%), and unchanged in hippocampus and putamen. In contrast, brain enzyme activity was normal in patients with the neurodegenerative disorder spinocerebellar ataxia type I. Our demonstration of ornithine decarboxylase activity in neonatal and adult human brain suggests roles for ornithine decarboxylase in both developing and mature brain function, and we provide further evidence for the involvement of abnormal polyamine system activity in Alzheimer's disease. Key Words: Human brain-Ornithine decarboxylase-Polyamine system-Development-Aging -Alzheimer's disease.

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“…How does lithium exert its effect? Lithium does not interfere directly with the activity of PA metabolizing enzymes (Matsui and Pegg, 1980;Richards et al, 1990;. Therefore, lithium must act on the intact cell and interfere with the generation of intracellular ''stress signal(s)" that turns on the PSR, probably at the transcriptional or posttranscriptional levels, but posttranslationa!…”

Section: Fig 3 Effects Of Chronic Intermittent Restraint Stress On Odcmentioning

confidence: 99%

“…Lithium has been implicated in the regulation of several signal transduction systems (Berridge et a!., 1989;Lachman and Papolos, 1989;Jope and Williams, 1994), but one mechanism, inhibition of the phosphoinositide signaling pathway, received special attention (Berridge et a!., 1989). However, lithium inhibition of the induction of ODC in cultured cells challenged with dexamethasone does not appear to occur via inhibition of the phosphoinositide signaling pathway (Richards et a!., 1990). It was recently shown that the inhibitory effect of lithium on phosphatidylinositol turnover in the brain is transient and disappears after chronic treatment (Hirvonen and Savolainen, 1991).…”

Section: Fig 3 Effects Of Chronic Intermittent Restraint Stress On Odcmentioning

confidence: 99%

Brain Polyamine Stress Response: Recurrence After Repetitive Stressor and Inhibition by Lithium

Gilad

1996

Journal of Neurochemistry

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We recently demonstrated that, unlike in peripheral tissues, the increase in activity of polyamine synthesizing enzymes observed in the brain after acute stress can be prevented by long-term, but not by short-term, treatment with lithium. In the present study we sought to examine the effects of chronic intermittent stress on two key polyamine synthesizing enzymes, ornithine decarboxylase and S-adenosylmethionine decarboxylase, and their modulation by lithium treatment. Adult male rats were subjected to 2 h of restraint stress once daily for 5 days and to an additional delayed stress episode 7 days later. Enzyme activities were assayed 6 h after the beginning of each stress episode. In contrast to the liver, where ornithine decarboxylase activity was increased (300% of the control) only after the first stress episode, the enzyme activity in the brain was increased after each stress episode (to~-~170% of the control). Unlike ornithine decarboxylase activity, S-adenosylmethionine decarboxylase activity was slightly reduced after the first episode (86% of the control) but remained unchanged thereafter. After cessation of the intermittent stress period, an additional stress episode 7 days later led again to an increase in ornithine decarboxylase activity in the brain (225% of the control) but not in the liver, whereas S-adenosylmethionine decarboxylase activity remained unchanged. The latter increase in ornithine decarboxylase activity was blocked by lithium treatment during the intervening 7day interval between stressors. The results warrant the following conclusions: (a) Repetitive application of stressors results in a recurrent increase in ornithine decarboxylase activity in the brain but to habituation of this response in the liver. (b) This brain polyamine stress response can be blocked by long-term (days) lithium treatment. (c) The study implicates an overreactive polyamine response as a component of the adaptive, or maladaptive, brain response to stressful events and as a novel molecular target for lithium action.

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Inhibition of hormone-stimulated ornithine decarboxylase activity by lithium chloride

Cited by 10 publications

References 26 publications

Review of lithium effects on immune cells

Review of lithium effects on immune cells

Ornithine Decarboxylase in Human Brain: Influence of Aging, Regional Distribution, and Alzheimer's Disease

Brain Polyamine Stress Response: Recurrence After Repetitive Stressor and Inhibition by Lithium

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