Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney

Abstract

Huang HS, Ma MC, Chen J. Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney. Am J Physiol Renal Physiol 295: F34-F45, 2008. First published September 17, 2008 doi:10.1152/ajprenal.90309.2008.-Vitamin E was previously reported to reduce calcium oxalate (CaOx) crystal formation. This study explored whether vitamin E deficiency affects intrarenal oxidative stress and accelerates crystal deposition in hyperoxaluria. The control (C) group of rats received a standard diet and drinking water, while the experimental groups received 0.75% ethylene glycol (EG) in drinking water for 42 days. Of the latter, one group received a standard diet (EG group), one received a low-vitamin E (LE) diet (EGϩLE group), and the last received an LE diet with vitamin E supplement (4 mg) (EGϩLEϩE group). The CϩLE and CϩLEϩE groups were the specific controls for the last two experimental groups, respectively. In a separate experiment, EG and EGϩLE rats were studied on days 3-42 to examine the temporal relationship between oxidative change and crystal formation. Urinary biochemistry and activity/levels of antioxidative and oxidative enzymes in glomeruli and tubulointerstitial specimens (TIS) were examined. In EG rats, CaOx crystal accumulation was associated with low antioxidative enzyme activity in TIS and with increased oxidative enzyme expression in glomeruli. In the EGϩLE group, marked changes in antioxidative and oxidative enzyme levels were seen and correlated with massive CaOx deposition and tubular damage. The increased oxidative stress seen with EGϩLE treatment was largely reversed by vitamin E supplementation. A temporal study showed that decrease in antioxidative defense and increased free radical formation in the EGϩLE group occurred before crystal deposition. This study shows that low vitamin E disrupts the redox balance and causes cell death, thereby favoring crystal formation. antioxidative proteins; free radicals; hyperoxaluria CALCIUM OXALATE (CaOx) crystal formation is a multifaceted and complex process that involves a series of chemical, physical, biochemical, and physiological events (6, 10, 16). The principal causative agent for the formation of calcium salt crystals is thought to be supersaturation that causes the precipitation of salts in urine. However, even though urine is supersaturated with calcium and oxalate ions in normal subjects, stones do not form because of the presence of inhibitors and other unknown mechanisms (22).Membrane injury is suggested to be the primary event in CaOx crystal binding, and oxalate-induced free radicals are significant causative factors in membrane injury (11,12,25). This injury leads to lipid and protein peroxidation and altered biochemical reactions, including depletion of the antioxidant defense system (25). On the basis of these findings, we hypothesized that if renal tubular injury due to increased oxidative stress caused by hyperoxaluria can be prevented, CaOx crystal accumulation in the kidneys can also be ...

Oral administration of indigenous oxalate degrading lactic acid bacteria and quercetin prevents calcium oxalate stone formation in rats fed with oxalate rich diet

“…Histopathological studies showed interstitial inflammation and high CaOx crystal deposition in the kidneys of rats fed with KOx diet. This result is concordant with previous study by Huang, Ma, and Chen (2009) who reported that oxidative stress and renal injury are associated with CaOx crystal deposition in hyperoxaluric rats, which is a crucial factor in crystal retention and subsequent stone formation. LAB administered rats showed normal morphology of renal tissue and decreased crystal deposition compared to rats fed with KOx.…”

Combination of vitamin E and vitamin C alleviates renal function in hyperoxaluric rats via antioxidant activity

“…Multifactorial conditions including oxalate-induced free radical production cause damaged tubular epithelial cells [11] which subsequently induce crystal deposition and stone formation [9]. Several studies also reported that crystal and stone can aggravate oxidative stress as well [8, 9, 12, 25, 27]. According to this, oxidative stress appears to be a vicious cycle for urolithiasis.…”

Oxalate: From the Environment to Kidney Stones

“…Recent studies have provided a more focused correlation between the oxalate-induced production of free radicals and effects of vitamin E. In rats fed with a vitamin E-defi cient diet accompanied by EG treatment, the formation of CaOx crystals intensified and their volume in urinary sediment increased causing atrophy and dilatation of tubules as well as interstitial cellular infi ltration. The administration of vitamin E ameliorated these effects, most likely due to its anti-oxidative properties (74,75). Vitamin B6 defi ciency increased the excretion of endogenous oxalate, which was further enhanced by adding glycine, deoxypyridoxine, and isonicotic acid hydrazide to the diet (76).…”