Interrelation of Platelet Vitamin E and Thromboxane Synthesis in Type I Diabetes Mellitus

Karpen, C.W.; Cataland, Samuel; O'Dorisio, Thomas M.; Panganamala, R.V.

doi:10.2337/diab.33.3.239

Cited by 48 publications

(19 citation statements)

References 14 publications

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“…31 These include decrease in plasma ascorbic acid levels, 32 33 intracellular deficiency of ascorbic acid (cellular scurvy), 34 and decrease in cellular vitamin E levels. 35 Moreover, ocular tissues probably have a higher free radical activity than any other organ, mainly because of ultraviolet exposure. 36 Higher levels of NO were found in the aqueous humour of diabetic patients and this may induce inflammatory reactions that cause cell damage.…”

Section: Discussionmentioning

confidence: 99%

Protective role of oral antioxidant supplementation in ocular surface of diabetic patients

Peponis

Papathanasiou²,

Kapranou³

et al. 2002

British Journal of Ophthalmology

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Aim: To investigate the effect of vitamin C and E supplementation in the levels of nitrite, nitric oxide (NO) related metabolite, and ocular surface parameters in diabetic patients. Methods: 50 patients with non-insulin dependent diabetes mellitus were given vitamin C (1000 mg/day) and vitamin E (400 IU/day) supplementation for 10 days. Nitrite levels in tears were measured by photometric determination before and after vitamin supplementation. Tear function parameters (Schirmer test I, BUT, ocular ferning test) and brush cytology analysis of the conjunctival epithelium were also evaluated. Results: Nitrite levels were found to be significantly reduced (p<0.05) after 10 days of vitamin C and E supplementation. Improved values for Schirmer test, BUT test, and ocular ferning test were also found. Goblet cell density and grading of squamous metaplasia showed a significant improvement. Conclusions: Oxidative stress and free radical production are elevated in diabetes mellitus. Antioxidants, such as vitamin C and vitamin E, probably have an important role in reducing the oxidative damage produced by nitric oxide and other free radicals and improving the ocular surface milieu.

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Section: Discussionmentioning

confidence: 99%

Protective role of oral antioxidant supplementation in ocular surface of diabetic patients

Peponis

Papathanasiou²,

Kapranou³

et al. 2002

British Journal of Ophthalmology

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“…The evidence includes the findings that plasma antioxidants such as ascorbic acid [28,29], vitamin E [30], uric acid [31] and glutathione [32] are all decreased in diabetes, but levels of plasma peroxides are elevated [33]. There also seems to be a link between diabetes and altered handling of transition metals [34][35][36][37], necessary catalysts of many oxidative processes.…”

Section: Introductionmentioning

confidence: 99%

Glucose oxidation and low-density lipoprotein-induced macrophage ceroid accumulation: possible implications for diabetic atherosclerosis

Hunt

Bottoms

Clare

et al. 1994

Biochemical Journal

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The exposure of proteins to high concentrations of glucose in vitro is widely considered a relevant model of the functional degeneration of tissue occurring in diabetes mellitus. In particular, the enhanced atherosclerosis in diabetes is often discussed in terms of glycation of low-density lipoprotein (LDL), the non-enzymic attachment of glucose to apolipoprotein amino groups. However, glucose can undergo transition-metal-catalysed oxidation under near-physiological conditions in vitro, producing oxidants that possess a reactivity similar to the hydroxyl radical. These oxidants can fragment protein, hydroxylate benzoic acid and induce lipid peroxidation in human LDL. In this study, glycation of LDL in vitro is accompanied by such oxidative processes. However, the oxidation of LDL varies with glucose concentration in a manner which does not parallel changes in protein glycation. Glycation increases in proportion to glucose concentration, whereas in our studies maximal oxidation occurs at a glucose concentration of approx. 25 mM. The modification of LDL resulting from exposure to glucose alters macrophage ceroid accumulation, a process which occurs in the human atherosclerotic plaque. The accumulation of ceroid in macrophages is shown to be related to LDL oxidation rather than LDL glycation, per se, as it too occurs at a maximum of approx. 25 mM. Oxidative sequelae of protein glycation appear to be a major factor in LDL-macrophage interactions, at least with respect to ceroid accumulation. Our observations are discussed in the context of the observed increase in the severity of atherosclerosis in diabetes.

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“…This elevated level of glutathione may be a protective mechanism since in diabetes, the levels of other antioxidants are reduced [7,8].…”

mentioning

confidence: 98%

Streptozotocin-induced diabetes is associated with increased renal lipoxygenase activity

Stewart

Whiting

Bell³

et al. 1998

Biochemical Society Transactions

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Diabetes is associated with increased renal production of vasodilator prostaglandins [ 1,2], which is postulated to mediate the hyperfiltration associated with the disease. While this hypothesis has been strengthened by the evidence that prostaglandin synthetase (PGS) inhibitors, lysine acetylsalicylate [3] & piroxicam [4], reduced the increased glomerular filtration rate (GFR) found in diabetic patients, other workers have found conflicting results [5]. A possible explanation for this discrepancy is that other eicosanoids, in addition to vasodilatory prostaglandins,are responsible for the altered renal haemodynamics associated with diabetes. Indeed we have previously shown that the kidney has high levels of lipoxygenase activity [6], which has the potential to generate other eicosanoids. We therefore decided to investigate renal lipoxygenase activity in diabetic rats.Sprague-Dawley rats were administered a single dose of streptozotocin (STZ) (45 mg/kg). The presence of diabetes was established 24 h later by the presence of frank glycosuria and polyuria. After 5 days, the rats were anaesthetised and blood removed by cardiac puncture. After cervical dislocation, kidneys were removed and subcellular fractions prepared.Blood analysis showed increased levels of glucose in the STZtreated animals compared with controls (29.9k3.1 ~s 8.3f1.2 mmoV1, n=4, ~4 . 0 1 ) . Similarly, creatinine levels increased in STZ-treated animals (75+6 ~s 53fl pnoUl, p<0.05), indicating impairment of glomerular function.Significantly higher levels of reduced glutathione (GSH) were observed in kidney cytosol from diabetic animals (107.4f31.6 ~s 5 1.8f1.8 nmolhg; p4.05). This elevated level of glutathione may be a protective mechanism since in diabetes, the levels of other antioxidants are reduced [7,8].PGS and lipoxygenase (LO) activity can be measured by investigation of the arachidonic acid (AA)-dependent metabolism of the model compound tetramethylphenylenediamine (TMPD) [9]. In the present study, we found that addition of AA (100p.M) caused a greater stimulation of activity in microsomes prepared from STZ-treated rats (16.8k2.1 nmol TMPD oxidisedmidmg) than that from controls (12.7M.7 nmoUmin/mg). The greater stimulation of AA-dependent activity in STZ-treated rats compared with controls (p

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Interrelation of Platelet Vitamin E and Thromboxane Synthesis in Type I Diabetes Mellitus

Cited by 48 publications

References 14 publications

Protective role of oral antioxidant supplementation in ocular surface of diabetic patients

Protective role of oral antioxidant supplementation in ocular surface of diabetic patients

Glucose oxidation and low-density lipoprotein-induced macrophage ceroid accumulation: possible implications for diabetic atherosclerosis

Streptozotocin-induced diabetes is associated with increased renal lipoxygenase activity

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