A Comparison of Modulation of Proliferation of Thymocyte by Testosterone, Dehydroisoandrosterone and Androstenedione in Vitro

Yao, Genhong; Shang, Xiaojing

doi:10.1080/014850190924115

Cited by 15 publications

(7 citation statements)

References 23 publications

(21 reference statements)

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“…However, Yao et al. [38] have demonstrated recently that the androgen structure is determinant in resulting in either the inhibition or the enhancement of LT proliferation. Thus, the authors have demonstrated that small structural changes of androgens (testosterone, DHEA or androstenedione) can result in markedly different biological effects.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have been carried out in order to elucidate the DHEA effects on the activation and proliferation of lymphocytes, but have resulted in controversial results [19,37]. However, Yao et al [38] have demonstrated recently that the androgen structure is determinant in resulting in either the inhibition or the enhancement of LT proliferation. Thus, the authors have demonstrated that small structural changes of androgens (testosterone, DHEA or androstenedione) can result in markedly different biological effects.…”

Section: Discussionmentioning

confidence: 99%

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Dehydroepiandrosterone and metformin regulate proliferation of murine T lymphocytes

Solano

Sander

Wald

et al. 2008

Clinical and Experimental Immunology

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SummaryThe aim of the present study was to assess the effect of dehydroepiandrosterone (DHEA: 10 mM) and metformin (10 mM and 100 mM) in regulating proliferation of cultured T lymphocytes. T cells were isolated from lymph nodes of prepuberal BALB/c mice. We found that DHEA, metformin and DHEA + metformin added to the incubation media diminished proliferation of T cells. The inhibition by DHEA was higher than that produced by metformin, while the combined treatment showed a synergistic action that allowed us to speculate distinct regulatory pathways. This was supported later by other findings in which the addition of DHEA to the incubation media did not modify T lymphocyte viability, while treatment with metformin and DHEA + metformin diminished cellular viability and increased both early and late apoptosis. Moreover, DHEA diminished the content of the antioxidant molecule glutathione (GSH), whereas M and DHEA + metformin increased GSH levels and diminished lipid peroxidation. We conclude that DHEA and metformin diminish proliferation of T cells through different pathways and that not only the increase, but also the decrease of oxidative stress inhibited proliferation of T cells, i.e. a minimal status of oxidative stress, is necessary to trigger cellular response.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone and metformin regulate proliferation of murine T lymphocytes

Solano

Sander

Wald

et al. 2008

Clinical and Experimental Immunology

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“…Conversion is usually more pronounced in young women and women with selected FMR1 genotypes/ subgenotypes (69). DHEA and testosterone also suppressed canavalin A (Con A)-induced proliferation of thymocytes in vitro, and DHEA is less potent than testosterone, which means that the balance between the two steroids can alter immune homeostasis (70). Testosterone and estradiol levels vary widely after DHEA administration, and the testosterone to estradiol ratio increased significantly in seven healthy nonobese postmenopausal women (71).…”

Section: Conversion To Other Steroidsmentioning

confidence: 99%

Dehydroepiandrosterone improves the ovarian reserve of women with diminished ovarian reserve and is a potential regulator of the immune response in the ovaries

Zhang

Gui

et al. 2015

BST

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“…Glucocorticoids, like the sex steroids, contribute to thymic involution (55), and DHEA has also been reported to have an apoptotic effect in thymic cells (68), while its metabolites androstenedione and DHEA-S have been reported to have opposite effects, with DHEA-S being antiapoptotic (70) and androstenedione stimulating thymocyte growth (69). The effect of thyroid hormone is biphasic with low doses being stimulatory (55), while too high doses may cause thymic atrophy (55).…”

Section: Introductionmentioning

confidence: 98%

The Spanish flu as a worst case scenario?

Moxnes¹,

Christophersen²

2008

Microbial Ecology in Health and Disease

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For preparation of pandemic plans for the H5N1 bird flu virus, it has been common practice among health authorities in several countries to use crude death figures from the Spanish flu pandemic as a worst case scenario. This has been done without taking into consideration either what is known about the molecular biology of malignant influenza viruses or the detailed statistical information that is available about the Spanish flu pandemic, as regards the variation of death risk as a function of age and also as regards the different behavior of the virus during successive pandemic waves. There is no scientific basis for the assumption that a new pandemic influenza virus cannot be worse than the Spanish flu virus. However, if we hypothetically assume recurrence of a pandemic influenza virus with virulence and transmissibility properties identical to the Spanish flu virus, but belonging to a subtype other than those that have been circulating in human populations since 1918, it will be unrealistic to assume that the older part of the population will be immune against a type of virus that their immune system has never encountered before. Therefore we have attempted to estimate what might have happened by counterfactually assuming that individuals in 1918 had not been immunized earlier against H1 (or H1N1) influenza viruses that were circulating before 1890. An overview is given of age-related changes in immunological factors that may affect the age-specific mortality in different age groups, and also expected consequences for the mortality in different age groups of mitochondrial DNA aging per se. Extrapolations for age-specific death rate have been made for four different scenarios, giving lower and upper boundaries for what might have happened if nobody had been immune when the 1918Á1920 pandemic started. For the first (lower boundary) scenario the age-specific death rate is increasing up to the age of 30 and is assumed (very unrealistically) to be constant thereafter. For the second scenario the age-specific death rate is monotonically increasing as a function of age according to an almost cubic functionality. For the third (upper boundary) scenario the agespecific death rate is increasing exponentially with age. For the third scenario the mortality of the world population becomes 0.3. Thus 30% of the world population could have been killed by the Spanish flu virus, had nobody been immune when the pandemic started. For the fourth scenario the mortality by age due to the virus mimics the traditional mortality by age in a population. The fifth scenario is identical with scenario 3, except that it is also counterfactually assumed that the wave 2 virus came first. For this scenario, it is found that as much as 80% of the total world population in 1918 might have been killed by the Spanish flu virus.

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A Comparison of Modulation of Proliferation of Thymocyte by Testosterone, Dehydroisoandrosterone and Androstenedione in Vitro

Cited by 15 publications

References 23 publications

Dehydroepiandrosterone and metformin regulate proliferation of murine T lymphocytes

Dehydroepiandrosterone and metformin regulate proliferation of murine T lymphocytes

Dehydroepiandrosterone improves the ovarian reserve of women with diminished ovarian reserve and is a potential regulator of the immune response in the ovaries

The Spanish flu as a worst case scenario?

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