ABSTRACT
Globally, cardiac arrest (CA) is a leading cause of death and disability. Asphyxial CA (ACA)-induced kidney damage is a crucial factor in reducing the survival rate. The purpose of this study was to investigate the role of antioxidant enzymes in histopathological renal damage in an ACA rat model at different time points. A total of 88 rats were divided into five groups and exposed to ACA except for the sham group. To evaluate glomerular function and oxidative stress, serum levels of blood urea nitrogen (BUN) and creatinine (Crtn) and malondialdehyde (MDA) levels in renal tissues were measured. To determine histopathological damage, hematoxylin and eosin staining, periodic acid-Schiff staining, and Masson's trichrome staining were performed. Expression levels of antioxidant enzymes including superoxide dismutase-1 (SOD-1), superoxide dismutase-2 (SOD-2), catalase (CAT), and glutathione peroxidase (GPx) were measured by immunohistochemistry (IHC). Survival rate of the experimental rats was reduced to 80% at 6 h, 55% at 12 h, 42.9% at 1 day, and 33% at 2 days after return of spontaneous circulation. Levels of BUN, Crtn, and MDA started to increase significantly in the early period of CA induction. Renal histopathological damage increased markedly from 6 h until two days post-CA. Additionally, expression levels of antioxidant enzymes were significantly decreased at 6 h, 12 h, 1 day, and 2 days after CA. CA-induced oxidative stress and decreased levels of antioxidant enzymes (SOD-1, SOD-2, CAT, GPx) from 6 h to two days could be possible mediators of severe renal tissue damage and increased mortality rate.
ABSTRACT
Aim: This study aimed to investigate the effects of nitrogen (NO3-N, NH3-N) and phosphorus (PO4-P) on the growth and microcystin production of two bloom-forming Microcystis species (toxic M. aeruginosa MAHC160824 and non-toxic M. viridis MVHC160824).Methodology: The two Microcystis species were isolated from the lower reaches of the Nakdong river, South Korea. In the culture experiments, the average nutrient concentrations (NH3-N, NO3-N and PO4-P) at which Microcystis appeared (> 15°C) was used as control medium. Different concentrations of NH3-N, NO3-N and PO4-P were then employed in nutrient testing (control, vs. 4 times and 16 times higher than the control). Microcystin levels were measured using a UPLC™ (LC MS/MS) system. Results: Both toxic and non-toxic Microcystis strains exhibited a maximum cell density at 30°C and a maximum growth rate at 25-30°C. In the nutrient addition assays, the maximum growth of two Microcystis species were found at nutrient concentrations 4 to 16 times higher than the control (NH3-N: 0.468 mg l-1, PO4-P: 0.100 mg l-1, NO3-N: 32.5 mg l-1). The highest microcystin production levels were found under optimal growth conditions. The microcystin levels of toxic M. aeruginosa MAHC160824 were below the detection limit despite a higher number of cells (> 300,000 cells ml-1) at the same nutrients concentrations as those found in raw water from the Nakdong river. Interpretation: Higher production of microcystin occurs when there is an increase in NH3-N and PO4-P within a restricted range in toxic species M. aeruginosa MAHC160824, else the production is low