Histological and functional renal alterations caused by Bothrops alternatus snake venom: Expression and activity of Na+/K+-ATPase

Linardi, Alessandra; Silva, Thomaz Augusto Alves da Rocha e; Miyabara, Elen Haruka; Franco‐Penteado, Carla F.; Cardoso, Kelen Cristiane; Bôer, Patrícia Aline; Moriscot, Anselmo Sigari; Gontijo, José Antônio Rocha; Joazeiro, Paulo Pinto; Collares-Buzato, Carla Beatriz; Hyslop, Stephen

doi:10.1016/j.bbagen.2011.06.006

Cited by 23 publications

(16 citation statements)

References 48 publications

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“…We observed tubular disruption especially in proximal tubules, necrosis in the glomerular and tubular areas, accumulation of collagen fibers in the necrotic areas, and mononuclear cell infiltration in renal tissue of rats treated with VPA (500 mg/kg/day) for 15 days. We also supported kidney injury findings by showing reduced activity of Na + /K + -ATPase which may indicate reduced renal function (Linardi et al 2011). Previously, it has been speculated that VPA might interact with sodium-dependent cotransporters such as Na + /K + -ATPase (Sirac et al 2011).…”

Section: Discussionsupporting

confidence: 86%

“…In addition, the activity of Na + /K + -ATPase was measured as an indicator of kidney injury since reduced activity of this enzyme is thought to be a sign of reduced renal function (Linardi et al 2011). Interestingly, vit U treatment given to intact rats reduced the activity of Na + /K + -ATPase (p<0.001, 3.48±0.23 in intact rats and 1.03±0.39 in Vit U-treated rats).…”

Section: Vit U Pretreatment Prevented Vpa-induced Renal Damagementioning

confidence: 99%

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Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties

et al. 2015

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The aim of present study was to investigate the effect of vitamin U (vit U, S-methylmethionine) on oxidative stress, inflammation, and fibrosis within the context of valproic acid (VPA)-induced renal damage. In this study, female Sprague Dawley rats were randomly divided into four groups: Group I consisted of intact animals, group II was given vit U (50 mg/kg/day, by gavage), group III was given VPA (500 mg/kg/day, intraperitonally), and group IV was given VPA + vit U. The animals were treated by vit U 1 h prior to treatment with VPA every day for 15 days. The following results were obtained in vit U + VPA-treated rats: (i) the protective effect of vit U on renal damage was shown by a significant decrease in histopathological changes and an increase in Na(+)/K(+)-ATPase activity; (ii) anti-oxidant property of vit U was demonstrated by a decrease in malondialdehyde levels and xanthine oxidase activity and an increase in glutathione levels, catalase and superoxide dismutase activities; (iii) anti-inflammatory property of vit U was demonstrated by a decrease in tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1 levels, and adenosine deaminase activity; (iv) anti-fibrotic effect of vit U was shown by a decrease in transforming growth factor-β, collagen-1 levels, and arginase activity. Collectively, these data show that VPA is a promoter of inflammation, oxidative stress, and fibrosis which resulted in renal damage. Vit U can be proposed as a potential candidate for preventing renal damage which arose during the therapeutic usage of VPA.

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Section: Discussionsupporting

confidence: 86%

Section: Vit U Pretreatment Prevented Vpa-induced Renal Damagementioning

confidence: 99%

Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties

et al. 2015

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“…Injured proximal tubule cells have alterations in the actin and microtubule cytoskeletal networks that lead to a redistribution of Na + /K + ATPase from the basolateral to the apical membrane, contributing to a decrease in Na + transport and reabsorption (Thadhani et al , 1996). It was reported that FE Na+ and FE K+ also increase in envenomation caused by Bothrops snakes (Boer-Lima et al , 1999; Linardi et al , 2011). Despite the redistribution of Na + /K + ATPase to the apical membrane, Linardi et al (2011) reported an increase in expression and activity of Na + /K + ATPase during envenomation by Bothrops alternatus and suggest that it is a protective mechanism triggered in response to natriuresis with the aim to preserve renal function during acute damage.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of acute kidney injury induced by experimental Lonomia obliqua envenomation

et al. 2014

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Background Lonomia obliqua caterpillar envenomation causes acute kidney injury (AKI), which can be responsible for its deadly actions. This study evaluates the possible mechanisms involved in the pathogenesis of renal dysfunction. Methods To characterize L. obliqua venom effects we subcutaneously injected rats and examined renal functional, morphological and biochemical parameters at several time points. We also performed discovery based proteomic analysis to measure protein expression to identify molecular pathways of renal disease. Results L. obliqua envenomation causes acute tubular necrosis, which is associated with renal inflammation; formation of hematic casts, resulting from intravascular hemolysis; increase in vascular permeability and fibrosis. The dilation of Bowman’s space and glomerular tuft is related to fluid leakage and intra-glomerular fibrin deposition, respectively, since tissue factor procoagulant activity increases in the kidney. Systemic hypotension also contributes to these alterations and to the sudden loss of basic renal functions, including filtration and excretion capacities, urinary concentration and maintenance of fluid homeostasis. In addition, envenomed kidneys increases expression of proteins involved in cell stress, inflammation, tissue injury, heme-induced oxidative stress, coagulation and complement system activation. Finally, the localization of the venom in renal tissue agrees with morphological and functional alterations, suggesting also a direct nephrotoxic activity. Conclusions Mechanisms of L. obliqua-induced AKI are complex involving mainly glomerular and tubular functional impairment and vascular alterations. These results are important to understand the mechanisms of renal injury and may suggest more efficient ways to prevent or attenuate the pathology of Lonomia’s envenomation.

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“…Functionally, B. alternatus venom induced oliguria, urine acidification, decreased in glomerular filtration rate and hematuria. Morphologically, the venom caused lobulation of the capillary tufts, dilation of Bowman's capsular space, disruption of renal tubule brush border, and fibrosis around glomeruli and proximal tubules that persisted 7 days after envenomation (Linardi et al, 2011;Mello et al, 2010). Some purified Bothrops toxins are able to reproduce the renal effects obtained with whole venom.…”

Section: Bothrops Venommentioning

confidence: 99%

Acute Kidney Injury Induced by Snake and Arthropod Venoms

Berger¹,

Vieira²,

Guimarães³

2012

Renal Failure - The Facts

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Histological and functional renal alterations caused by Bothrops alternatus snake venom: Expression and activity of Na+/K+-ATPase

Abstract: Enhanced Na+/K+-ATPase activity in the early hours after envenoming may attenuate the renal dysfunction associated with venom-induced damage.

Cited by 23 publications

References 48 publications

Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties

Vitamin U has a protective effect on valproic acid-induced renal damage due to its anti-oxidant, anti-inflammatory, and anti-fibrotic properties

Mechanisms of acute kidney injury induced by experimental Lonomia obliqua envenomation

Acute Kidney Injury Induced by Snake and Arthropod Venoms

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