Glucose May Induce Cell Death through a Free Radical-Mediated Mechanism

Donnini, Debora; Zambito, Anna Maria; Perrella, Giuseppina; Ambesi-Impiombato, Francesco Saverio; Curcio, Francesco

doi:10.1006/bbrc.1996.0247

Cited by 60 publications

(34 citation statements)

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“…The elevated blood glucose levels in diabetes are thought to lead to cell death through oxidative stress induction that occurs as a common sequel of diabets-induced modification of sugar moieties on proteins and lipids (Donnini et al, 1996). Hyperglycemia increases oxidative stress through the overproduction of reactive oxygen species, which results in an imbalance between free radicals and the antioxidant defense systems of the cells.…”

Section: Discussionmentioning

confidence: 99%

Antidiabetic activities of ethanol extract of dry matters of culture broth of Coriolus versiolor in submerged culture

Zhang¹,

Lv²,

Pan³

et al. 2011

Braz. arch. biol. technol.

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The study aimed to investigate the antihyperglycemic and antilipidperoxidative effects of ethanol extract of the dry matter from culture broth of Coriolus versicolor (ECBC) in streptozotocin-induced diabetes mice. Blood glucose level, insulin level, total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol(LDL-C), high density lipoprotein -cholesterol (HDL-C) in serum and reduced glutathione level (GSH), lipid peroxidation

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Section: Discussionmentioning

confidence: 99%

Antidiabetic activities of ethanol extract of dry matters of culture broth of Coriolus versiolor in submerged culture

Zhang¹,

Lv²,

Pan³

et al. 2011

Braz. arch. biol. technol.

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“…In these animal models when hyperglycaemia is allowed to continue, a so-called ªglucotoxicityº to beta cells impairs insulin secretion [2,16,17] and eventually causes fatal islet cell injury, accelerating beta-cell loss [2,17]. Aggravated hyperglycaemia with sucrose feeding provokes excessive oxidative stress that has been associated with an increased rate of apoptosis in pancreatic beta cells in Type II diabetic animal models [18,19].…”

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confidence: 99%

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

et al. 2002

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Impaired insulin secretion and insulin resistance are a characteristic feature of Type II (non-insulin-dependent) diabetes mellitus [1,2]. In spite of extensive studies on the pathophysiology of diabetes, islet pathology and its pathogenesis remain controversial.Classical studies using histochemical methods to identify endocrine cells have reported varying results, including the severe loss of beta cells [3], modest changes with amyloid deposition [4,5] and even no change of islet beta-cell population [6]. Immunohistochemical techniques for the identification of specific populations of islet endocrine cells, showed a nearly 50 % reduction in beta-cell volume density in European Type II non-obese diabetic patients compared with non-diabetic control subjects [7]. Other studies have reported a 24 % reduction of islet beta-cell area density, a 58 % increase in A cell area density and a deposition of amyloid that correlated with the severity of islet pathology [8]. In another study of European Type II diabetic patients, a separate research group has reported Diabetologia (2002) Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients Abstract Aims/hypothesis. We examined the pancreatic islet lesions in Japanese patients with Type II diabetes mellitus to determine if the damage was related to oxidative stress. Methods. Morphometric analyses were performed on immunostained sections of the tail portion of the pancreas from 14 diabetic and 15 non-diabetic patients. Amyloid deposition and oxidative stress-induced tissue damage were evaluated by Congo-red staining and immunostaining. Resistance to oxidative stress was assessed from immunostaining results for Cu, Zn-superoxide dismutase (SOD). Expression of (pro)insulin mRNA was assessed by in situ hybridisation. Results. The pancreas from diabetic patients had amyloid deposition in about 15 % of the islets, intensified reactions of 8-OHdG and HNE, as well as reduced expression of SOD. Islet volume density of beta cells and total beta-cell mass in the pancreas from diabetic patients were reduced by 22 % (p < 0.001) and 30 % (p < 0.05). Islet volume density and total mass of (pro)insulin mRNA-positive cells were similarly reduced in diabetic patients by 22 % (p < 0.001) and 39 % (p < 0.05), respectively. Islet volume density of A cells was increased by 20 % (p < 0.001) but total mass did not change. There were no changes in volume densities of islet, D and PP cells. Reduced beta-cell volume density correlated with increased positive staining of 8-OHdG. Conclusion/interpretation. Japanese Type II diabetic patients show a reduction of beta-cell mass and evidence of increased oxidative stress-related tissue damage that is correlated with the extent of the beta-cell lesions. [Diabetologia (2002) 45: 85±96]

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“…Although glucose-induced oxidative stress possibly is important in promoting VSMC growth, there is little doubt that oxidative stress can also induce cell death [18]; therefore both the degree of oxidant stress and cell type must have potential importance in the growth response. Endogenous antioxidant defences to protect against attack by reactive oxygen species include the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) and the non-enzymatic aqueous phase antioxidant glutathione, which is perhaps the most important and versatile protector [19].…”

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The effects of glucose-induced oxidative stress on growth and extracellular matrix gene expression of vascular smooth muscle cells

et al. 1998

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Diabetes mellitus is a major risk factor for atherosclerosis. In population based studies diabetes is associated with an increased incidence of coronary heart disease [1], cerebrovascular disease and peripheral vascular disease [2]. The high prevalence of macrovascular disease is partly explained by the increased frequency of conventional risk factors and partly by risk factors specific for diabetes including hyperglycaemia, hyperinsulinaemia and dyslipidaemia. The view that diabetic vasculopathy is, at least in part, related to excess free radicals is supported by evidence such as increased lipid peroxidation [3] and reduced antioxidant reserve in patients with diabetes [4] and from studies showing a direct cytotoxic effect of free Diabetologia (1998) Summary Vascular smooth muscle cell (VSMC) dysfunction plays a role in diabetic macrovasculopathy and this may include abnormalities in growth characteristics and the extracellular matrix. As the actual mechanisms by which glucose induces VSMC dysfunction remain unclear, the aim of this study was to assess the potential role of glucose-induced oxidative stress. Porcine aortic VSMCs were cultured for 10 days in either 5 mmol/l normal glucose or 25 mmol/l D-glucose (high glucose). There was evidence of oxidative stress as indicated by a 50 % increase in intracellular malondialdehyde (p < 0.05), increased mRNA expression of CuZn superoxide dismutase and Mn superoxide dismutase (by 51 % and 37 % respectively, p < 0.01) and a 50 % decrease in glutathione in 25 mmol/l D-glucose (p < 0.001). Growth was increased by 25.0 % (p < 0.01). mRNA expression of extracellular matrix proteins (collagens I, III, IV and fibronectin) was not altered by high glucose in these experimental conditions. Repletion of glutathione with N-acetyl L-cysteine (1 mmol/l) in VSMC grown in high glucose was associated with reduction in malondialdehyde and restored growth to that of normal glucose. The water soluble analogue of vitamin E, Trolox (200 mmol/l), reduced malondialdehyde concentrations, but had no effect on glutathione depletion or the increased growth rate seen with high glucose. The addition of buthionine sulphoximine (10 mmol/l) to VSMC cultured in normal glucose reduced glutathione, increased malondialdehyde and increased growth to a similar extent as that found in high glucose alone. These results suggest that thiol status, rather than lipid peroxides, is a key factor in modulating VSMC growth and that mRNA expression of extracellular matrix proteins is not increased in VSMC under conditions of glucose-induced oxidative stress. [Diabetologia (1998

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Glucose May Induce Cell Death through a Free Radical-Mediated Mechanism

Cited by 60 publications

References 0 publications

Antidiabetic activities of ethanol extract of dry matters of culture broth of Coriolus versiolor in submerged culture

Antidiabetic activities of ethanol extract of dry matters of culture broth of Coriolus versiolor in submerged culture

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients

The effects of glucose-induced oxidative stress on growth and extracellular matrix gene expression of vascular smooth muscle cells

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