Membrane ion transport systems during oxidative stress in rodent brain: Protective effect of stobadine and other antioxidants

Lehotský, Ján; Kaplán, Peter; Račay, Peter; Matejovičová, Milena; Drgová, A; Mézesová, V

doi:10.1016/s0024-3205(99)00454-3

Cited by 63 publications

(38 citation statements)

References 29 publications

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“…The present study showed that peroxidation of lipids was significantly increased in the liver of diabetic rats, which in turn resulted in elevated production of other free radicals that are harmful to the cell (55) . Hypoinsulinaemia during diabetes increased the oxidation of fatty acids and resulted in decreased membrane fluidity, changed the activity of membrane-bound enzymes and receptors, impaired Ca metabolism (56) , elevated the level of TAG and LDL-cholesterol and reduced the level of HDL-cholesterol, which led to liver dysfunction (57) . Antioxidant enzymes, SOD and GPx, have an important role in maintaining physiological levels of free radicals by hastening the dismutation of free radicals and eliminating organic peroxides and H 2 O 2 (10) .…”

Section: Discussionmentioning

confidence: 99%

Effect of vitamin D₃in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

George¹,

Kumar

Antony

et al. 2012

Br J Nutr

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Diabetes mellitus is a growing health problem worldwide and is associated with severe liver complications. The aim of the present study is to analyse the status of metabolic and free-radical-scavenging enzymes and second messengers in the liver of streptozotocin (STZ)-induced diabetic rats, and to determine the hepatoprotective role of vitamin D 3 . All studies were performed using the liver of adult male Wistar rats. Gene expression studies were carried out using real-time PCR with specific probes. Second messenger levels were determined using 3 H-labelled Biotrak assay kits, and glucose uptake assay with D-[ 14 C]glucose. The present results show that there was a decrease in hepatic glucose uptake, malate dehydrogenase activity, glycogen content, inositol triphosphate (IP 3 ) and cyclic GMP levels, and superoxide dismutase, glutathione peroxidase, phospholipase C, cyclic AMP-responsive element-binding protein, vitamin D receptor (VDR) and insulin receptor (INSR) gene expression in the diabetic rats when compared with the controls (all P,0·05), while cyclic AMP levels and GLUT2 expression were increased (P,0·05). Treatment of the diabetic rats with vitamin D 3 and insulin reversed the altered parameters to near control values. In conclusion, the data suggest a novel role of vitamin D 3 in restoring impaired liver metabolism in STZ-induced diabetic rats by regulating glucose uptake, storage and metabolism. We demonstrated that the restoring effect of vitamin D 3 is mediated through VDR modulation, thereby improving signal transduction and controlling free radicals in the liver of diabetic rats. These data suggest a potential role for vitamin D 3 in the treatment of diabetes-associated hepatic complications.Key words: Vitamin D: Diabetes: Liver: Oxidative stress: Metabolism: Insulin Diabetes-associated complications are major causes of morbidity and mortality. The liver plays a unique role in glucose homeostasis. Because of its anatomical location, it is ideally suited to control the systemic supply of absorbed nutrients, and it is one of only two organs that both consume and produce substantial amounts of glucose. The central role of the liver in the maintenance of blood glucose levels is assured by complex regulation by metabolic substrates, insulin and other hormones (1) . Diabetes-associated hyperglycaemia and hypoinsulinaemia lead to the impairment of hepatic glucose and lipid metabolism. Virtually, the entire spectrum of liver diseases is seen in patients with diabetes, including liver cirrhosis, a significant cause of death in diabetic patients, even more relevant than CVD (2) . Interest in the development of novel antidiabetic agents has been fuelled by the intense complications due to therapeutic treatment of diabetes and associated liver failure (2,3) . An increased prevalence of diabetes has been observed in vitamin D-deficient individuals (4) , and our previous study has shown that vitamin D 3 treatment restores blood glucose homeostasis in streptozotocin (STZ)-induced diabetic rats (5) . Bind...

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Section: Discussionmentioning

confidence: 99%

Effect of vitamin D₃in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

George¹,

Kumar

Antony

et al. 2012

Br J Nutr

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“…The inactivation of Na + -K + ATPase leads to partial membrane depolarization allowing excessive Ca 2+ entry inside neurons with resultant toxic events like excitotoxicity (Shepherd 1994;Beal 1995). This membrane bound enzyme requires phospholipid for its activity and is highly vulnerable to oxidative insult and the mechanism of inactivation under such conditions involves disruption of phospholipid microenvironment of the enzyme or direct damage to enzyme protein by reactive oxygen radicals or lipid peroxidation products (Lehtosky et al 1999). There are reports that the activity of Na + -K + ATPase declines in brain of aged animals although the cause of this decline is not clearly established (Tanaka and Ando 1990;Viani et al 1991).…”

Section: Introductionmentioning

confidence: 99%

Membrane Associated Functions of Neurokinin B (NKB) on Aβ (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes

et al. 2006

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The effect of different concentrations (0.1-5 microM) of neurokinin B (NKB) and Abeta (25-35) on acetylcholine esterase (AChE), Na(+)-K(+) ATPase and membrane fluidity (DPH anisotropy) were investigated in rat brain synaptosomes of 3, 9, 18 and 30 months old. An age dependent decrease was observed for all the three parameters studied. An in vitro incubation of isolated brain synaptosomes with Abeta (25-35) showed toxic effects on all the parameters studied and the peptide had concentration and age dependent effects, while NKB showed stimulating effect on the parameters and the combined NKB+Abeta (25-35) incubations showed a partial reversal effect as compared to the Abeta (25-35) alone. Thus, the results suggest a membrane mediated function for NKB and its role in neuromodulation, neuroprotection and antioxidant property against Abeta (25-35) induced toxicity in aging brain functions.

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“…One of the main aims of the study of Pavlikova et al (2009) was to determine whether IRI and IPC would affect the physical and functional properties of hippocampal membrane vesicles including Golgi SP. Neuronal microsomes are vulnerable to physical and functional oxidative damage (Lehotsky et al 1999(Lehotsky et al , 2002aUrikova et al 2006). The nature of the effect of free radicals on SPCA1 protein is not yet known.…”

Section: Effect Of Oxidative Damage On Spca1mentioning

confidence: 99%

“…SP are involved in the stress sensing, neuronal aging and transduction of apoptotic signals (Maag et al, 2003;Sepulveda et al, 2008). In order to evaluate whether the severe metabolic stress induced by IRI and/or IPC affects transcription of SPCA1 gene, the mRNA and protein levels of SPCA1 was analyzed (Lehotsky, 1999(Lehotsky, , 2002a(Lehotsky, , 2004. As shown by Pavlikova et al (2009), RT-PCR clearly detected, that hippocampal cells respond to the IRI by induction of mRNA level in reperfusion period with maximum at 3 h reperfusion (to 171% of control).…”

Section: Effect Of Oxidative Damage On Spca1mentioning

confidence: 99%

“…Preconditioning (IPC) initiates earlier tissue response to the injury by the significant elevation of mRNA expression already at 1 h of reperfusion and the level of mRNA expression reached 142% comparing to 1 h ischemia, and to 164% comparing to control. Neuronal microsomes are vulnerable to physical and functional oxidative damage (Lehotsky et al, 1999(Lehotsky et al, , 2002a(Lehotsky et al, , 2004Urikova et al, 2006). The authors showed that SPCA activity, similar to other P-type ATPases, is also subject to ischemic damage most likely due to free radicals action (Lehotsky et al, 2002b).…”

Section: Effect Of Oxidative Damage On Spca1mentioning

confidence: 99%

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Mechanisms of Ischemic Induced Neuronal Death and Ischemic Tolerance

Lehotský¹,

Pavlíková²,

Straka³

et al. 2012

Advances in the Preclinical Study of Ischemic Stroke

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Membrane ion transport systems during oxidative stress in rodent brain: Protective effect of stobadine and other antioxidants

Cited by 63 publications

References 29 publications

Effect of vitamin D₃in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

Effect of vitamin D₃in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

Membrane Associated Functions of Neurokinin B (NKB) on Aβ (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes

Mechanisms of Ischemic Induced Neuronal Death and Ischemic Tolerance

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Membrane ion transport systems during oxidative stress in rodent brain: Protective effect of stobadine and other antioxidants

Cited by 63 publications

References 29 publications

Effect of vitamin D3in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

Effect of vitamin D3in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

Membrane Associated Functions of Neurokinin B (NKB) on Aβ (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes

Mechanisms of Ischemic Induced Neuronal Death and Ischemic Tolerance

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Effect of vitamin D₃in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats

Effect of vitamin D₃in reducing metabolic and oxidative stress in the liver of streptozotocin-induced diabetic rats