Table 6 shows that the LD50 of vBj decreased the content of GSH and increased the content of GSSG and the value of the GSSG/GSH index in the renal cortex and medulla. SA was efficient to restore the normal levels of GSSG and GSH in the renal cortex and medulla of envenomed mice. LA was efficient to increase the levels of GSH in the cortex of envenomed mice. Overall, SA and LA were efficient to restore the normal value of the GSSG/GSH index in the renal cortex
and medulla of envenomed mice. AKI implies a rapid development of renal dysfunction that is characterized by oliguria or anuria with decreased abilities of excretion, urinary concentration and homeostasis of Epacadostat in vivo body fluids (Schrier et al., 2004). All renal structures can be involved, but the acute tubular necrosis is most commonly observed in the hemodynamic disruption, immune reactions and nephrotoxicity induced by snake envenomation (Burdmann, 1989, Monteiro STAT inhibitor et al., 2001, Azevedo-Marques et al., 2003, França and Málaque, 2003 and Castro et al., 2004). The LD50 of vBj was preconized as AKI inducer ( Rezende et al., 1989). In fact, the present study shows that all envenomed mice with this dose of vBj exhibited alterations in renal function,
including the increase of plasma creatinine, which has been used as the main index of acute renal failure ( Gomes et al., 2002 and Saravia et al., 2002). Regarding the absence of a uniform and precise characterization of acute renal failure, the ADQI (Acute Dialysis Analytic Initiative) group organized, in 2002, the formation and evaluation of a data bank with parameters of renal patients, in order to propose Teicoplanin consensual normative diagnostic parameters for acute renal failure. This study also aimed to improve the therapeutic resources for acute renal failure. Thus, in 2008, the AKIN (Acute Kidney Injury Network) group suggested that the detection of alterations in absolute levels of serum creatinine, plasma urea and urinary volume would be the prominent criteria to identify acute renal failure ( Cerdá et al., 2008, Davenport
et al., 2008 and Mehta et al., 2007). However, limitations impede the acceptance of rigid criteria to define acute renal failure, since there is a general diversity in the clinical and laboratorial conditions of renal patients. Data from Yamasaki et al. (2008) and Alegre et al. (2010), for example, have suggested that hyperuricemia (that appears before glomerular damage, since only part of envenomed animals had hypercreatinemia) and urinary hypoosmolality (together with hypercreatinemia, a small decrease in plasma urea and increased hematocrit) are the main characteristics of acute renal failure induced in mice by ip injection of the venom of the snake C. d. terrificus. As evidenced in the present study, the hyperuricemia and hypercreatinemia are both equally incidents in the AKI induced in mice by the venom of B.
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