Increased apoptosis in a variety of tissues of zinc-deficient rats

Nodera, Makoto; Yanagisawa, Hiroyuki; Wada, Osamu

doi:10.1016/s0024-3205(01)01252-8

Cited by 62 publications

(52 citation statements)

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“…This effect resulted from a direct action of zinc on the mitochondrial release of cytochrome c followed by caspase activation and cascading apoptotic events (Feng et al, 2000;. In contrast, most reports with other mammalian cells describe a role of zinc in the inhibition of apoptosis (Truong-Tran et al, 2000;Nodera et al, 2001). The most likely reason for this is that the levels of zinc to which the cells were exposed were lower and exposed time of cells was shorter than that of the present work.…”

Section: +contrasting

confidence: 70%

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

Yang

Sun

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To evaluate effects of epigallocatechin-3-gallate (EGCG) on the viability, membrane properties, and zinc distribution, with and without the presence of Zn . The proportion of EGCG incorporated into liposomes treated with the mixture of EGCG and Zn 2+ at the ratio of 1:1 was 90.57%, which was significantly higher than that treated with EGCG alone (30.33%). Electron spin resonance (ESR) studies and determination of fatty acids showed that the effects of EGCG on the membrane fluidity of LNCaP were decreased by Zn 2+. EGCG accelerated the accumulation of zinc in the mitochondria and cytosol as observed by atomic absorption spectrometer. Conclusion: These results show that EGCG interacted with cell membrane, decreased the membrane fluidity of LNCaP cells, and accelerated zinc accumulation in the mitochondria and cytosol, which could be the mechanism by which EGCG inhibits proliferation of LNCaP cells. In addition, high concentrations of Zn 2+ could attenuate the actions elicited by EGCG.

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Section: +contrasting

confidence: 70%

Epigallocatechin-3-gallate affects the growth of LNCaP cells via membrane fluidity and distribution of cellular zinc

Yang

Sun

et al. 2009

J. Zhejiang Univ. Sci. B

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“…The main phenotypic feature of this depletion is the loss of immature CD4 þ CD8 þ cells, a finding consistently seen in malnutrition secondary to protein, metal element -including zinc, magnesium and iron -or vitamin deficiency diets (Chandra, 1992;Kuvibidila et al, 1990;Dhur et al, 1991;Malpuech-Brugere et al, 1999). As recently demonstrated in rats exposed to deficiencies of Mg or Zn, the consequent thymocyte depletion actually reflects a massive apoptosis of these cells in the organ (Malpuech-Brugere et al, 1999;Nodera et al, 2001).…”

Section: Phenotypic and Functional Changes Of Thymocytes In Malnutritionmentioning

confidence: 80%

The thymus gland is a target in malnutrition

2002

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Malnutrition, secondary to deficiency in uptake of proteins, metal elements or vitamins, consistently results in changes in the thymus gland. The organ undergoes a severe atrophy due to apoptosis-induced thymocyte depletion, particularly affecting the immature CD4 þ CD8 þ cells, as well as a decrease in cell proliferation. Such a feature is apparently linked to a hormonal imbalance, involving decrease of leptin and consequent raise of glucocorticoid hormone levels in the serum. Interestingly, this picture can be reversed after appropriate diet rehabilitation. The thymic microenvironment is also affected in malnutrition: morphological changes in thymic epithelial cells were found, together with a decrease of thymic hormone production by these cells. Additionally, intrathymic contents of extracellular proteins, such as fibronectin, laminin and collagens, are increased in the thymuses from malnourished children. Conjointly, the bulk of data discussed herein clearly points to the notion that the thymus gland is a target in malnutrition. Nevertheless, further relevant information regarding the physiology of the thymus, including the cytokine=chemokine secretion as well as the positive and negative selection events driven by TCR=MHC-peptide interactions in malnutrition, remains to be defined. These are questions that need to be answered in order to have a better understanding of the immunodeficiency seen in malnourished individuals.

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“…Li et al [1998] observed a significant (P < 0.01) increase in apoptotic number of spermatogenic cells after zinc deficiency. Nodera et al [2001] also reported the appearance of TUNEL positive cells after 3 w of zinc deficiency in testes and thymus of 7 w old Sprague Dawley rats. Abnormally accelerated apoptosis of germ cells may lead to an imbalance of cell proliferation and death resulting in spermatogenic impairment [Takagi et al 2001;Kimura et al 2003].…”

Section: Groupsmentioning

confidence: 92%