Alpha-tocopherol protects against the renal damage caused by potassium dichromate

Arreola-Mendoza, Laura; Reyes, José L.; Meléndez-Camargo, María Estela; Martín, Dolores; Namorado, María C.; Sánchez, Elsa; Razo, Luz M. Del

doi:10.1016/j.tox.2005.11.010

Cited by 36 publications

(42 citation statements)

References 45 publications

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“…Urinary protein to creatinine ratio was obtained by dividing urine protein concentration by urine creatinine concentration, both expressed in mg/dL. Urinary and serum Na + and K + concentrations were measured by atomic absorption spectrophotometry (Perkin Elmer 3100 with an air- acetylene flame, Norwalk, CT, USA) as previously described [29]. Na + and K + fractional excretion were calculated according to the following equation: Fractional excretion of Na + or K + (%) = (Na + or K + clearance/creatinine clearance) x 100.…”

Section: Methodsmentioning

confidence: 99%

Aldosterone signaling regulates the over-expression of claudin-4 and -8 at the distal nephron from type 1 diabetic rats

et al. 2017

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Hyperglycemia in diabetes alters tight junction (TJ) proteins in the kidney. We evaluated the participation of aldosterone (ALD), and the effect of spironolactone (SPL), a mineralocorticoid receptor antagonist, on the expressions of claudin-2, -4, -5 and -8, and occludin in glomeruli, proximal and distal tubules isolated from diabetic rats. Type 1 diabetes was induced in female Wistar rats by a single tail vein injection of streptozotocin (STZ), and SPL was administrated daily by gavage, from days 3–21. Twenty-one days after STZ injection the rats were sacrificed. In diabetic rats, the serum ALD levels were increased, and SPL-treatment did not have effect on these levels or in hyperglycemia, however, proteinuria decreased in SPL-treated diabetic rats. Glomerular damage, evaluated by nephrin and Wilm’s tumor 1 (WT1) protein expressions, and proximal tubular damage, evaluated by kidney injury molecule 1 (Kim-1) and heat shock protein 72 kDa (Hsp72) expressions, were ameliorated by SPL. Also, SPL prevented decrement in claudin-5 in glomeruli, and claudin-2 and occludin in proximal tubules by decreasing oxidative stress, evaluated by superoxide anion (O2●―) production, and oxidative stress markers. In distal tubules, SPL ameliorated increase in mRNA, protein expression, and phosphorylation in threonine residues of claudin-4 and -8, through a serum and glucocorticoid-induced kinase 1 (SGK1), and with-no-lysine kinase 4 (WNK4) signaling pathway. In conclusion, this is the first study that demonstrates that ALD modulates the expression of renal TJ proteins in diabetes, and that the blockade of its actions with SPL, may be a promising therapeutic strategy to prevent alterations of TJ proteins in diabetic nephropathy.

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Section: Methodsmentioning

confidence: 99%

Aldosterone signaling regulates the over-expression of claudin-4 and -8 at the distal nephron from type 1 diabetic rats

et al. 2017

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“…In the same study it was observed that administration of all-trans-retinoic acid, the active form of vitamin A, reduced the elimination of living cells [36]. Arreola-Mendoza et al [37] reported that in addition to damage to proximal tubules demonstrated by increased excretion of glucose and decreased capacity of the secretory pathway of organic anions, distal functions of the nephron, as water regulation, were altered by this metal. Arreola-Mendoza et al [38] confirmed in the same model that Cr severely altered expression and distribution of occludin and claudin 2; α -tocopherol, active form of vitamin E, protected renal cells from damage induced by this metal, through the participation of extracellular signal-regulated kinase 1/2 (ERK1/2).…”

Section: Nephrotoxicity Of Heavy Metals On Tjsmentioning

confidence: 99%

“…Lipoperoxidation is produced in different regions of kidney and it is attenuated by the α -tocopherol [37, 38]. …”

Section: Oxidative and Nitrosative Stress In Kidneymentioning

confidence: 99%

Tight Junction Proteins and Oxidative Stress in Heavy Metals-Induced Nephrotoxicity

Reyes

Molina‐Jijón

Rodríguez-Muñóz

et al. 2013

BioMed Research International

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Kidney is a target organ for heavy metals. They accumulate in several segments of the nephron and cause profound alterations in morphology and function. Acute intoxication frequently causes acute renal failure. The effects of chronic exposure have not been fully disclosed. In recent years increasing awareness of the consequences of their presence in the kidney has evolved. In this review we focus on the alterations induced by heavy metals on the intercellular junctions of the kidney. We describe that in addition to the proximal tubule, which has been recognized as the main site of accumulation and injury, other segments of the nephron, such as glomeruli, vessels, and distal nephron, show also deleterious effects. We also emphasize the participation of oxidative stress as a relevant component of the renal damage induced by heavy metals and the beneficial effect that some antioxidant drugs, such as vitamin A (all-trans-retinoic acid) and vitamin E (α-tocopherol), depict on the morphological and functional alterations induced by heavy metals.

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“…Cephaloridine cytotoxicity was also inhibited by probenecid (30,33), a specific inhibitor of the renal PAH transport. In a model of acute renal failure, treatment with vitamin E preserved proximal reabsorptive and secretory functions (34).…”

Section: Discussionmentioning

confidence: 99%

Protection against cephalosporin-induced lipid peroxidation and nephrotoxicity by (+)-cyanidanol-3 and vitamin E

Cojocel

Tolle

El-Hajj

et al. 2007

Braz J Med Biol Res

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The ability of the clinically used cephalosporins: cephalothin, cefotaxime and cefotiam to induce lipid peroxidation (LPO) and renal damage was compared to that of nephrotoxic cephaloridine under in vivo conditions. Glutathione was measured in rat liver or in renal cortex as non-protein sulfhydryls. LPO was measured in plasma, renal cortex and liver by the generation of malondialdehyde or as the increase in renal cortical concentration of conjugated dienes. Impairment of renal function was measured as the decrease in renal cortical accumulation of the organic anion p-aminohippurate (PAH). Administration of cephalosporins to rats as a single dose (2000 mg/kg, ip) induced a significant glutathione-depletion in the renal cortex with cephaloridine, and in the liver with cephaloridine, cephalothin and cefotiam. Treatment of rats with cephaloridine, cephalothin and cefotiam (200, 500, or 1000 mg kg -1 day -1 , ip) for 5 days resulted in a dose-dependent increase of LPO in the renal cortex. While cephaloridine induced the highest concentration of conjugated diene, cefotaxime had no effect. Measurements of PAH accumulation in renal cortical slices from cephalosporin-treated rats showed a dose-dependent decrease in the renal cortical accumulation of PAH. Pretreatment with the antioxidants vitamin E or cyanidanol (400 mg kg -1 day -1 , ip) 1 h before treatment with cephaloridine, cephalothin or cefotiam (1000 mg kg -1 day -1 , ip) for 3 days inhibited cephalosporin-induced LPO and significantly reduced the impairment of renal cortical accumulation of PAH. The potential of different cephalosporins for inducing LPO and reducing PAH accumulation was ranked as follows: cephaloridine > cephalothin > cefotiam > cefotaxime.

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Alpha-tocopherol protects against the renal damage caused by potassium dichromate

Cited by 36 publications

References 45 publications

Aldosterone signaling regulates the over-expression of claudin-4 and -8 at the distal nephron from type 1 diabetic rats

Aldosterone signaling regulates the over-expression of claudin-4 and -8 at the distal nephron from type 1 diabetic rats

Tight Junction Proteins and Oxidative Stress in Heavy Metals-Induced Nephrotoxicity

Protection against cephalosporin-induced lipid peroxidation and nephrotoxicity by (+)-cyanidanol-3 and vitamin E

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