Decrease of Thymic Hormone Serum Level in Cockayne Syndrome

Bensman, A; Dardenne, Mireille; Jf, Bach; J, Valleteau de Mouillac; Lasfargues, G.

doi:10.1203/00006450-198202000-00002

Cited by 6 publications

(3 citation statements)

References 11 publications

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“…We showed that the in vitro chelation, followed by incubation of Zn2+-deprived mice sera with ZnC12 induced a full recovery of thymulin biological activity. Similar observations were made with sera from children presenting nephrotic syndrome with Zn2+ deficiency [19], a disease in which we observed a low level of thymulin activity that could be restored to normal after in vitro chelation and incubation with ZnC12 [8]. These results confirm the presence of the inactive hormone in the serum of Zn2+-deficient mice or individuals and its potential activation following Zn2+ addition.…”

Section: Discussionsupporting

confidence: 91%

“…More recently, several investigators evoked the possibility that the epithelial function of the thymus may be specifically altered by this nutritional deficiency. They reported that a Zn2+ deficit induced a significant lowering of the serum level of thymic hormone, thymulin (previously called serum thymic factor, ITS), both in animal models such as mice and rats [5,61 and in patients with common variable immunodeficiency [7] or nephrotic syndrome with zinc deficiency [8]. Moreover, Zn administration restored normal hormone levels.…”

Section: Introductionmentioning

confidence: 97%

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In vivo and in vitro studies of thymulin in marginally zinc‐deficient mice

et al. 1984

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Thymulin (or serum thymic factor, FTS-Zn), a well-defined thymic hormone previously shown to be a nonapeptide binding the metal zinc, was studied in mice subjected to a long-term marginally Zn-deficient diet. In spite of the absence of thymic atrophy, we observed a significant decrease in the serum levels of thymulin as early as two months after the onset of treatment. However, these levels could be consistently restored after in vitro addition of ZnCl2. The analysis of thymuses from Zn-deficient mice showed that, despite the apparently normal network of epithelial cells, there was a progressive increase in the number of thymulin -containing cells (assessed by immunofluorescence with anti- thymulin monoclonal antibodies) that was already significant after two months of treatment. These results are in keeping with those of previous investigators, showing a specific, altered, thymic endocrine function following Zn deprivation. Nonetheless, our results strongly suggest that the nonactive Zn-deprived peptide is secreted under these experimental conditions. Furthermore, the fact that the augmented numbers of thymulin -containing cells were observed in the thymuses following a decrease in the peripheral thymulin (biologically active) brings further evidence for the existence of a feedback mechanism for the secretion of this hormone.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 97%

In vivo and in vitro studies of thymulin in marginally zinc‐deficient mice

et al. 1984

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“…We and other groups recently studied thymulin levels in various pathological situations with zinc deficiency the first study was performed in young children with nephrotic syndrome where we observed low thymulin levels, compared to age-matched subjects. These low levels of thymulin activity were restored to normal after remission of the disease or after in vitro addition of zinc salts to the serum under study (32). In addition, we performed similar studies in subjects with sickle cell anemia.…”

Section: Zinc Deficiency In Pathological Situationsmentioning

confidence: 79%

Interactions Between Zinc and Thymulin

Dardenne

Pleau

1994

Metal-Based Drugs

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Cockayne syndrome: Review of 140 cases

1992

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To define diagnostic criteria for Cockayne Syndrome (CS) and to identify in detail the complications of the condition, a comprehensive review of 140 cases of CS was performed. Criteria required for the diagnosis include poor growth and neurologic abnormality; other very common manifestations include sensorineural hearing loss, cataracts, pigmentary retinopathy, cutaneous photosensitivity, and dental caries. The mean age of death in reported cases is 12 3/12 years, though a few affected individuals have lived into their late teens and twenties. Prenatal growth failure, congenital structural eye anomalies, severe neurologic dysfunction from birth, and the presence of cataracts within the first 3 years of life are predictors of severe disease and early death. In contrast with other disorders of chromosome or DNA repair, cancer has never been reported in a classical CS patient, and there appears to be no predisposition to infectious complications. The wide spectrum of symptoms and severity of the disease suggest that biochemical and genetic heterogeneity exist. CS is an uncommon but devastating genetic condition which will be better understood as the biochemical interrelationships between DNA replication and repair, and between growth, homeostasis, and oncogenesis are unraveled.

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Decrease of Thymic Hormone Serum Level in Cockayne Syndrome

Cited by 6 publications

References 11 publications

In vivo and in vitro studies of thymulin in marginally zinc‐deficient mice

In vivo and in vitro studies of thymulin in marginally zinc‐deficient mice

Interactions Between Zinc and Thymulin

Cockayne syndrome: Review of 140 cases

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