Nutr Res Pract.  2014 Feb;8(1):46-53.

Nephroprotective effect of astaxanthin against trivalent inorganic arsenic-induced renal injury in wistar rats

Affiliations
  • 1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. zhangzhigang@neau.edu.cn

Abstract

Inorganic arsenic (iAs) is a toxic metalloid found ubiquitously in the environment. In humans, exposure to iAs can result in toxicity and cause toxicological manifestations. Arsenic trioxide (As2O3) has been used in the treatment for acute promyelocytic leukemia. The kidney is the critical target organ of trivalent inorganic As (iAsIII) toxicity. We examine if oral administration of astaxanthin (AST) has protective effects on nephrotoxicity and oxidative stress induced by As2O3 exposure (via intraperitoneal injection) in rats. Markers of renal function, histopathological changes, Na+-K+ ATPase, sulfydryl, oxidative stress, and As accumulation in kidneys were evaluated as indicators of As2O3 exposure. AST showed a significant protective effect against As2O3-induced nephrotoxicity. These results suggest that the mechanisms of action, by which AST reduces nephrotoxicity, may include antioxidant protection against oxidative injury and reduction of As accumulation. These findings might be of therapeutic benefit in humans or animals suffering from exposure to iAsIII from natural sources or cancer therapy.

Keyword

Astaxanthin; trivalent inorganic arsenic; arsenic accumulation; nephrotoxicity; oxidative stress

MeSH Terms

Adenosine Triphosphatases
Administration, Oral
Animals
Arsenic
Humans
Kidney
Leukemia, Promyelocytic, Acute
Oxidative Stress
Rats
Rats, Wistar*
Adenosine Triphosphatases
Arsenic

Figure

  • Fig. 1 Effect of AST and As2O3 on activities of SOD (A), CAT (B), and MDA levels (C) in renal tissues. Values represent the mean ± SE, for 8 rats in each group. *P < 0.01 vs the control group, #P < 0.05 vs the As2O3-treated group (As2O3: 5 mg/kg BW). L: AST: 10 mg/kg BW, As2O3: 5 mg/kg BW. M: AST: 20 mg/kg BW, As2O3: 5 mg/kg BW. H: AST: 40 mg/kg BW, As2O3: 5 mg/kg BW.

  • Fig. 2 Effect of AST and As2O3 on ROS (A) and 8-OHdG (B) levels in renal tissues. Values represent the mean ± SE, for 8 rats in each group. *P < 0.01 vs the control group, #P < 0.05 vs the As2O3-treated group (As2O3: 5 mg/kg BW). L: AST: 10 mg/kg BW, As2O3: 5 mg/kg BW. M: AST: 20 mg/kg BW, As2O3: 5 mg/kg BW. H: AST: 40 mg/kg BW, As2O3: 5 mg/kg BW.

  • Fig. 3 Effects of AST and As2O3 on the levels of GSH (A) and ratios of GSH/GSSG (B) in renal tissues. Values represent the mean ± SE, for 8 rats in each group. *P < 0.01 vs the control group, #P < 0.05 vs the As2O3-treated group (As2O3: 5 mg/kg BW). L: AST: 10 mg/kg BW, As2O3: 5 mg/kg BW. M: AST: 20 mg/kg BW, As2O3: 5 mg/kg BW. H: AST: 40 mg/kg BW, As2O3: 5 mg/kg BW.

  • Fig. 4 Hematoxylin and eosin-stained kidney slices from the treated rats. The control rats (A) with normal morphology. The As2O3-treated rats (B) with damaged kidney structure. The As2O3-treated rats fed with AST (C-E) with reduced effects of As2O3 toxicity on the renal tissues. The As2O3+AST-treated rats (AST: 10 mg/kg BW; As2O3: 5 mg/kg BW) (C), As2O3+AST-treated rats (AST: 20 mg/kg BW; As2O3: 5 mg/kg BW) (D), As2O3+AST-treated rats (AST: 40 mg/kg BW; As2O3: 5 mg/kg BW) (E). Original magnification: 200×.

  • Fig. 5 Effect of AST and As2O3 on the total As accumulation in renal tissues. Values represent the mean ± SE, for 8 rats in each group. *P < 0.01 vs the control group, #P < 0.05 vs the As2O3-treated group (As2O3: 5 mg/kg BW). L: AST: 10 mg/kg BW, As2O3: 5 mg/kg BW. M: AST: 20 mg/kg BW, As2O3: 5 mg/kg BW. H: AST: 40 mg/kg BW, As2O3: 5 mg/kg BW.


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