Vitamin E ameliorates enhanced renal lipid peroxidation and accumulation of F2-isoprostanes in aging kidneys

1998 ◽  
Vol 274 (3) ◽  
pp. R767-R774 ◽  
Author(s):  
Jane F. Reckelhoff ◽  
Vijaya Kanji ◽  
Lorraine C. Racusen ◽  
Ann Marie Schmidt ◽  
Shu Du Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Renal Function ◽  
Vitamin E ◽  
Heme Oxygenase ◽  
Control Diet ◽  
Glomerular Sclerosis ◽  
High Vitamin ◽  
Age Related ◽  
Renal Aging

Aging results in progressive glomerular sclerosis and reductions in glomerular filtration rate (GFR). Oxidative stress may be an important mechanism for the aging process, but to date the role of oxidative stress on renal aging has not been determined. The present study was performed to determine whether age-related alterations in renal hemodynamics and morphology were associated with oxidative stress and whether this could be attenuated by chronic administration of vitamin E. Rats, aged 13 mo, were given either control diet containing vitamin E 50 IU/kg ( n = 6) or a high-vitamin E diet (5,000 IU/kg; n = 6) for 9 mo. Another group of rats (3–4 mo old; n = 7) served as young controls. Aging was accompanied by a 60% reduction in GFR, a threefold increase in renal F2 isoprostanes, newly discovered vasoconstrictive F2-like prostaglandins generated by free radical-mediated lipid peroxidation. Renal aging was also associated with an increase in oxidant-sensitive heme oxygenase, advanced glycosylation end products (AGEs), and the AGE receptor, RAGE. AGE-RAGE interaction has been shown to induce oxidative stress. With high-vitamin E diet, GFR was increased by 50%, F2 isoprostanes were suppressed, and expression of heme oxygenase and RAGE was attenuated. There was also a tendency for glomerular sclerosis to be attenuated. These data demonstrate that age-related decline in renal function is accompanied by oxidative stress and that administration of antioxidants, such as vitamin E, could attenuate the decline in renal function.

scholarly journals Zone-specific damage of the olfactory epithelium under protein restriction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ayinuer Tuerdi ◽  
Shu Kikuta ◽  
Makoto Kinoshita ◽  
Teru Kamogashira ◽  
Kenji Kondo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Olfactory Epithelium ◽  
Control Diet ◽  
Intervention Strategy ◽  
Protein Restriction ◽  
Outer Hair Cells ◽  
Basal Cells ◽  
Cell Dynamics ◽  
Age Related ◽  
Positive Effect

AbstractOxidative stress causes tissue damage, affecting age-related pathologies. Protein restriction (PR) provides a powerful intervention strategy for reducing oxidative stress, which may have a positive effect on individual organs. However, it is unknown whether PR intervention influences the olfactory system. Here, we investigated how 10 months of PR could affect the cell dynamics of the olfactory epithelium (OE) in mice. We found that PR reduced age-related loss of outer hair cells in the cochlea, providing preventive effects against age-related hearing loss. In contrast, PR resulted in reduced mature olfactory sensory neurons (OSNs), increased proliferative basal cells, and increased apoptotic OSNs in zone 1 (the only area containing neurons expressing NQO1 [quinone dehydrogenase 1]) of the OE in comparison with animals given a control diet. Substantial oxidative stress occurred in NQO1-positive cells and induced apoptotic OSNs in zone 1. These results indicate that in contrast to the positive effect on the auditory system, PR induces oxidative stress and structurally and functionally negative effects on OSNs in zone 1, which is probably involved in the bioactivation of NQO1.

Acute lead exposure induces renal haeme oxygenase-1 and decreases urinary Na excretion

2003 ◽  
Vol 22 (5) ◽  
pp. 237-244 ◽  
Author(s):  
Hilda Vargas ◽  
Carlos Castillo ◽  
Francisco Posadas ◽  
Bruno Escalante
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Renal Function ◽  
Lead Exposure ◽  
Lead Acetate ◽  
Single Injection ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Tin Protoporphyrin ◽  
Pb Exposure

The effects of acute lead exposure on renal function, lipid peroxidation and the expression of haeme oxygenase (HO) in rat kidney were determined. A single injection of lead acetate (50 mg Pb/kg) was given to rats. Changes in renal function, characterized by a significant reduction in the Na excretion was observed six hours after Pb exposure; this effect persisted for 24 hours. TBARS levels increased in kidney cortex 24 hours after Pb administration. In kidney cortex, Pb exposure affected the expression of HO-1, a renal protein associated with oxidative stress. HO-1 mRNA increased 2.3-fold, three hours after Pb administration and remained increased for six, 12 and 24 hours. HO enzymatic activity and HO-1 protein increased six and three hours after Pb administration, respectively, and remained increased at 24 hours. HO inhibition by tin-protoporphyrin, potentiated Pb-induced increase in TBARS and prevented the Pb-induced reduction in Na excretion. Our data suggest that Pb may be acting through the generation of oxidant products and induction of HO.

Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney

2008 ◽  
Vol 295 (2) ◽  
pp. R543-R549 ◽  
Author(s):  
Analía Lorena Tomat ◽  
Felipe Inserra ◽  
Luciana Veiras ◽  
María Constanza Vallone ◽  
Ana María Balaszczuk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Systolic Blood Pressure ◽  
Zinc Deficiency ◽  
Control Diet ◽  
Adult Life ◽  
Fetal Life ◽  
Arterial Blood ◽  
End Products

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.

Effect of curcumin on hepatic heme oxygenase 1 expression in high fat diet fed rats: is there a triangular relationship?

2014 ◽  
Vol 92 (10) ◽  
pp. 805-812 ◽  
Author(s):  
Yıldız Öner-İyidoğan ◽  
Sevda Tanrıkulu-Küçük ◽  
Muhammed Seyithanoğlu ◽  
Hikmet Koçak ◽  
Semra Doğru-Abbasoğlu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Liver ◽  
Heme Oxygenase ◽  
High Fat Diet ◽  
Control Diet ◽  
Heme Oxygenase 1 ◽  
High Fat ◽  
Curcumin Treatment ◽  
Fat Accumulation ◽  
Hepatic Fat

High fat diet (HFD) is associated with oxidative stress induced fatty liver. Curcumin, an extract of Curcuma longa, has been shown to possess potent antioxidant and hypolipidemic properties. In this study, we investigated the effect of curcumin treatment on hepatic heme oxygenase-1 (HO-1) expression along with pro-oxidant–antioxidant status and lipid accumulation in rats fed an HFD. Male Sprague–Dawley rats were distributed among 4 groups: Group 1, which was fed the control diet (10% of total calories from fat); Group 2, which was fed the HFD (60% of total calories from fat); and groups 3 and 4, which received the HFD supplemented with curcumin and the control diet supplemented with curcumin (1 g/kg diet; w/w), respectively, for 16 weeks. HFD caused increases in hepatic lipid levels, production of reactive oxygen species, and lipid peroxidation. Further, HO-1 expression was significantly decreased. Histopathological examination showed hepatic fat accumulation and slight fibrotic changes. Curcumin treatment reduced hepatic lipids and oxidative stress parameters, and HO-1 expression was significantly increased. These findings suggest that increased HO-1 expression, along with suppressed oxidative stress as well as reduced hepatic fat accumulation and fibrotic changes, contribute to the beneficial effects of curcumin in attenuating the pathogenesis of fatty liver induced metabolic diseases.

Re-evaluation of the vitamin E requirements of juvenile tilapia (Oreochromis niloticus ✕ O. aureus)

2001 ◽  
Vol 72 (3) ◽  
pp. 529-534 ◽  
Author(s):  
S. Y. Shiau ◽  
L. F. Shiau
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Oreochromis Niloticus ◽  
Control Diet ◽  
Dietary Treatment ◽  
Dietary Lipid ◽  
Tocopheryl Acetate ◽  
Dietary Vitamin ◽  
Feeding Trial ◽  
Protein Deposition

AbstractA 10-week feeding trial was conducted to re-evaluate the level of dietary vitamin E (DL- α-tocopheryl acetate) that was adequate for juvenile tilapia Oreochromis niloticus ✕ O. aureus given diets containing two dietary lipid concentrations. Purified diets with eight levels of vitamin E (0, 25, 50, 75, 100, 150, 200, 400 mg/kg diet) at either 50 or 120 g lipid per kg were each given to three replicate groups of tilapia (mean weight: 0·69 (s.e.0·02) g) reared in a closed, recirculating system. Food efficiency and protein deposition were significantly (P < 0·05) higher in fish given 50 mg vitamin E per kg diet and 75 mg/kg diet in the 50 and 120 g lipid per kg groups respectively, compared with fish given the unsupplemented control diet. Mortality of fish was not affected by dietary treatment. Weight gain and liver microsomal ascorbic acid-stimulated lipid peroxidation data analysed by broken-line regression indicated that the optimum dietary vitamin E requirements in juvenile tilapia are 42 to 44 mg vitamin E per kg and 60 to 66 mg vitamin E per kg in 50 and 120 g lipid per kg diets, respectively.

Effects of vitamin E supplementation on exercise-induced oxidative stress: a meta-analysis

2014 ◽  
Vol 39 (9) ◽  
pp. 1029-1037 ◽  
Author(s):  
Vahan Stepanyan ◽  
Melissa Crowe ◽  
Nagaraja Haleagrahara ◽  
Bruce Bowden
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin E ◽  
Muscle Damage ◽  
Meta Analysis ◽  
Protective Effects ◽  
Study Selection ◽  
Exercise Induced ◽  
Study Designs ◽  
Selection Of

Tocopherols (commonly referred to as “vitamin E”) are frequently studied antioxidants in exercise research. However, the studies are highly heterogeneous, which has resulted in contradicting opinions. The aim of this review is to identify similar studies investigating the effects of tocopherol supplementation on exercise performance and oxidative stress and to perform minimally biased qualitative comparisons and meta-analysis. The literature search and study selection were performed according to Cochrane guidelines. A 2-dimensional study execution process was developed to enable selection of similar and comparable studies. Twenty relevant studies were identified. The high variability of study designs resulted in final selection of 6 maximally relevant studies. Markers of lipid peroxidation (malondialdehyde) and muscle damage (creatine kinase) were the 2 most frequently and similarly measured variables. Meta comparison showed that tocopherol supplementation did not result in significant protection against either exercise-induced lipid peroxidation or muscle damage. The complex antioxidant nature of tocopherols and low accumulation rates in muscle tissues could underlie an absence of protective effects.

scholarly journals Lipid Peroxidation-Derived Aldehydes, 4-Hydroxynonenal and Malondialdehyde in Aging-Related Disorders

Antioxidants ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 102 ◽  
Author(s):  
Giuseppina Barrera ◽  
Stefania Pizzimenti ◽  
Martina Daga ◽  
Chiara Dianzani ◽  
Alessia Arcaro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Structural Damage ◽  
Membrane Lipids ◽  
Biological Fluids ◽  
Second Messengers ◽  
Biological Macromolecules ◽  
Age Related ◽  
Distinct Cell ◽  
Reactive Aldehydes

Among the various mechanisms involved in aging, it was proposed long ago that a prominent role is played by oxidative stress. A major way by which the latter can provoke structural damage to biological macromolecules, such as DNA, lipids, and proteins, is by fueling the peroxidation of membrane lipids, leading to the production of several reactive aldehydes. Lipid peroxidation-derived aldehydes can not only modify biological macromolecules, by forming covalent electrophilic addition products with them, but also act as second messengers of oxidative stress, having relatively extended lifespans. Their effects might be further enhanced with aging, as their concentrations in cells and biological fluids increase with age. Since the involvement and the role of lipid peroxidation-derived aldehydes, particularly of 4-hydroxynonenal (HNE), in neurodegenerations, inflammation, and cancer, has been discussed in several excellent recent reviews, in the present one we focus on the involvement of reactive aldehydes in other age-related disorders: osteopenia, sarcopenia, immunosenescence and myelodysplastic syndromes. In these aging-related disorders, characterized by increases of oxidative stress, both HNE and malondialdehyde (MDA) play important pathogenic roles. These aldehydes, and HNE in particular, can form adducts with circulating or cellular proteins of critical functional importance, such as the proteins involved in apoptosis in muscle cells, thus leading to their functional decay and acceleration of their molecular turnover and functionality. We suggest that a major fraction of the toxic effects observed in age-related disorders could depend on the formation of aldehyde-protein adducts. New redox proteomic approaches, pinpointing the modifications of distinct cell proteins by the aldehydes generated in the course of oxidative stress, should be extended to these age-associated disorders, to pave the way to targeted therapeutic strategies, aiming to alleviate the burden of morbidity and mortality associated with these disturbances.

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