Regulation of Apoptosis by Vitamin C

Vissers, Margreet C.M.; Lee, Wai Gin; Hampton, Mark B.

doi:10.1074/jbc.m107664200

Cited by 63 publications

(10 citation statements)

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“…[47] Vissers et al reported that intracellular ascorbate can specifically protect apoptosis in human umbilical vein endothelial cells (HUVEC) in the presence of chlorinated oxidants. [48] In the present study, a significant decrease in the severity of histopathological and morphometric changes induced by cisplatin was observed in rat kidney treated with vitamin C plus cisplatin when compared with the cisplatin group.…”

Section: Discussionmentioning

confidence: 66%

Protective Effects of Vitamin C on Cisplatin-Induced Renal Damage: A Light and Electron Microscopic Study

2008

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The present study was performed to investigate whether the chronic administration of antioxidant vitamin C provided morphological protection on cisplatin-induced renal damage. Wistar albino male rats were divided into control and two experiment groups, each consisting of six rats. Cisplatin (5 mg/kg/ month) was administered intravenously to the second and third group for three months. After the first application of cisplatin, vitamin C (8 mg/kg/day) to the third group was administered intramuscular for 3 months. At the end of the third month, the kidney specimens of the all groups were obtained. All of these kidney specimens were processed for light and electron microscopical examination. In the second group, most of the renal corpuscle lost their normal appearance and size, especially in the corticomedullary region. The most obvious changes were encountered in the proximal tubules. These changes were tubular dilation, thickening of basement membrane, loss of brush border, vacuolization, and swollenness of mitochondria in the proximal tubule epithelial cells. In addition, infiltration foci were observed mainly in the cortical region. In the third group, which was administered cisplatin plus vitamin C, although the structural damages and morphometric changes were lessened, mononuclear cell infiltration was still observed. This study suggests that the chronic administration of vitamin C may be of therapeutic benefit on cisplatin nephrotoxicity.

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Section: Discussionmentioning

confidence: 66%

Protective Effects of Vitamin C on Cisplatin-Induced Renal Damage: A Light and Electron Microscopic Study

2008

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“…It has been demonstrated that the apoptosis-inducing activity of ascorbate in human myelogenous leukemic cell lines is abrogated by catalase, implicating the involvement of hydrogen peroxide [56]. However, studies by Vissers et al [57] in human umbilical vein endothelial cells treated with chlorinated oxidants showed that although ascorbate (1mM) was ineffective at preventing glutathione oxidation or protecting against the cytotoxicity of these agents, it appeared to protect the apoptotic machinery from oxidant damage, allowing progression of apoptosis over necrosis. Here, we have demonstrated a similar but more modest effect in macrophages, even in the presence of catalase and using a 10-fold lower and more physiologically relevant concentration [58] of ascorbate.…”

Section: Discussionmentioning

confidence: 86%

Ascorbate does not protect macrophages against apoptosis induced by oxidised low density lipoprotein

Harris

Mann

Ruiz

et al. 2006

Archives of Biochemistry and Biophysics

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Apoptosis of macrophages and smooth muscle cells is observed in atherosclerotic lesions and may play an important role in the disease progression. Oxidised low density lipoprotein (LDL) is cytotoxic and induces apoptosis in a variety of cell types. We reported previously that ascorbate protects arterial smooth muscle cells from apoptosis induced by oxidised LDL containing the peak levels of lipid hydroperoxides. We now demonstrate that macrophages undergo apoptosis when treated with this species of oxidised LDL, as detected by increased annexin V binding and DNA fragmentation. Ascorbate treatment of macrophages did not protect against the cytotoxicity of oxidised LDL, and modestly increased the levels of annexin V binding and DNA fragmentation. Oxidised LDL treatment also increased the expression of the antioxidant stress protein heme oxygenase-1 in macrophages; however, this increase was markedly attenuated by ascorbate pretreatment. Although apoptosis induced by oxidised LDL was modestly promoted by ascorbate, ascorbate apparently decreased the levels of oxidative stress in macrophages, suggesting that this pro-apoptotic effect was not mediated by a pro-oxidant mechanism, but may instead have been due to intracellular protection of the apoptotic machinery by ascorbate.

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“…The oxidative process helps exposure of phosphatidylserine on antibody-damaged neutrophils, so that they are phagocytosed [83]. Yet actually chloramine dampens this process [84] and could explain the impaired neutrophil clearance [85], which will mean that antigens could persist to induce autoantibody formation. However, excessive ROS production by neutrophils can also lead to hyporesponsive T lymphocytes [86].…”

Section: Pathophysiological Implicationsmentioning

confidence: 99%