A new C-type animal lectin isolated from Bothrops pirajai is responsible for the snake venom major effects in the isolated kidney

We investigated the biochemical and biological effects of a new C-type galactoside specific lectin termed BPL that was isolated from the snake venom of Bothrops pirajai. This lectin was purified using size exclusion HPLC followed by an immobilized lactose affinity column. The purified BPL was homogeneous by reverse phase HPLC and SDS-PAGE. We evaluated the nephrotoxicity of the whole venom of B. pirajai and its lectin. The whole venom of B. pirajai (10 μg/mL) showed similar results as those observed for BPL (3, 10 and 30 μg/mL) evaluated by the perfused rat kidney method. They caused reductions in perfusion pressure (Control120 = 110.28 ± 3.69; BP120 = 70.70 ± 2.40∗; BPL3120 = 113.20 ± 4.40; BPL10120 = 67.80 ± 3.00∗; BPL30120 = 64.90 ± 3.50∗ mmHg; ∗: P <0.05), renal vascular resistance, urinary flow, glomerular filtration rate (Control90 = 0.695 ± 0.074; BP90 = 0.142 ± 0.032∗; BPL390 = 0.314 ± 0.064; BPL1090 = 0.250 ± 0.038∗; BPL3090 = 0.088 ± 0.021∗ mL g−1 min−1; ∗: P < 0.05) and sodium (Control120 = 81.28 ± 0.26; BP120 = 55.71 ± 5.72∗; BPL3120 = 80.94 ± 0.93; BPL10120 = 65.23 ± 1.47∗; BPL30120 = 76.03 ± 1.70∗%; ∗: P < 0.05), potassium and chloride tubular transport. Neither whole venom nor purified BPL induced direct vasoactive effects in perfused arteriolar mesenteric bed, and BPL did not potentiate bradykinin contraction in the ileum. We postulate that both B. pirajai and BPL promoted the same renal effects probably caused by the release of inflammatory mediators.