2008
DOI: 10.1016/j.toxicon.2007.08.017
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Purification and renal effects of phospholipase A2 isolated from Bothrops insularis venom

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Cited by 16 publications
(4 citation statements)
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“…AKI is 10 times more common in crotalic accidents than in bothropic, but the incidences are similar due to the greater number of accidents caused by the Bothrops genus [ 31 , 36 ]. Venom toxins have direct renal action, changing their structure [ 30 , 38 40 ] and physiology [ 41 ] due to capillary vulnerability. Moreover, Acute Tubular Necrosis (ATN) is the most common cause of AKI in snakebite envenomation [ 38 , 42 , 43 ].…”
Section: Introductionmentioning
confidence: 99%
“…AKI is 10 times more common in crotalic accidents than in bothropic, but the incidences are similar due to the greater number of accidents caused by the Bothrops genus [ 31 , 36 ]. Venom toxins have direct renal action, changing their structure [ 30 , 38 40 ] and physiology [ 41 ] due to capillary vulnerability. Moreover, Acute Tubular Necrosis (ATN) is the most common cause of AKI in snakebite envenomation [ 38 , 42 , 43 ].…”
Section: Introductionmentioning
confidence: 99%
“…PLA 2 s have a pivotal role in inflammation by activating arachidonic acid that leads to generation of eicosanoids (prostaglandins and leukotrienes). They also stimulate the hypothalamicpituitary-adrenal axis to produce adrenocorticotropic hormone, corticosteroids, vasopressin and acute phase proteins; as well as cause local manifestations at the bite site and hemodynamic changes [43,[45][46][47][48]. SVSPs are highly expressed in kidneys.…”
Section: Bothrops Venommentioning
confidence: 99%
“…The pathogenesis of AKI remains poorly described, but factors such as bleeding, inflammatory processes, fibrin deposition in the renal tubules, immune complexes formation, and the venom's direct action may be related [ 18 , 21 – 23 ]. Studies with different Bothrops species have shown that BaV can lead to renal damage and proximal tubular damage after the bite [ 22 , 24 ]. In addition, cytokines can be released by leukocytes and renal tubular cells after cell injury and are important components of the initiation and extension of inflammation in AKI [ 25 ].…”
Section: Introductionmentioning
confidence: 99%