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Updated: May 24, 2026
Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Single sublethal dose of microcystin-LR is responsible for different alterations in biochemical, histological and
J Lowe1, J Souza-Menezes, D S Freire
1Laboratory of Biological Physical Chemistry, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Abstract:
Microcystins (MCYSTs) are very stable cyclic peptidic toxins produced by cyanobacteria. Their effects on hepatic tissue have been studied extensively, and they are considered to be a potent hepatotoxin. However, several effects of MCYST on other organs have also been described, but generally in studies using higher doses of MCYST. In the present work, we investigated the effect of a single sublethal dose of MCYST-LR (55 μg/kg) in Wistar rats and analyzed different aspects that influenced renal physiology, including toxin accumulation, excretion, histological morphology, biochemical responses and oxidative damage in the kidney. After 24 h of exposure to MCYST-LR, it was possible to observe an increased glomerular filtration rate (6.28 ± 1.56 vs 2.16 ± 0.48 μl/min per cm(2)) compared with the control group. Increase of interstitial space and collagen deposition corresponded to a fibrotic response to the increased production of reactive oxygen species. The observed decrease of Na(+) reabsorption was due to inhibition of the activity of both Na(+) pumps in proximal tubules cells. We suggested that this modulation is mediated by the effect of MCYST as a phosphatase protein inhibitor that maintains the sustained kinase-mediated regulatory phosphorylation of the ATPases. The observed alteration of Na(+) active transporters lead to damage of renal function, since are involved in regulation of water and solute reabsorption in proximal tubules. The results of this report reinforce the importance of understanding the molecular effects of a single sublethal dose of MCYST-LR, which, in this study, was responsible for macro-alterations found in the renal parenchyma and renal physiology in rats.
Insights
A single sublethal dose of microcystin-LR (MCYST-LR) significantly impacts rat kidney function. This cyanotoxin exposure caused increased glomerular filtration, fibrosis, and impaired sodium reabsorption, highlighting renal risks.
Area of Science:
- Environmental Toxicology
- Nephrology
- Biochemistry
Background:
- Microcystins (MCYSTs) are stable cyanobacterial toxins primarily known as hepatotoxins.
- Previous studies on MCYST effects on organs other than the liver often used higher doses.
- The renal effects of sublethal MCYST exposure require further investigation.
Purpose of the Study:
- To investigate the renal physiological and histological effects of a single sublethal dose of MCYST-LR in Wistar rats.
- To analyze MCYST-LR accumulation, excretion, and its impact on kidney biochemistry and oxidative stress.
Main Methods:
- Administration of a single sublethal dose of MCYST-LR (55 μg/kg) to Wistar rats.
- 24-hour post-exposure analysis of glomerular filtration rate, renal histology, and biochemical markers.
- Assessment of Na(+) pump activity and oxidative damage indicators in kidney tissue.
Main Results:
- Increased glomerular filtration rate (GFR) observed 24 hours post-exposure.
- Histological analysis revealed interstitial space expansion and collagen deposition, indicating fibrosis.
- Decreased Na(+) reabsorption due to inhibition of Na(+) pump activity in proximal tubules, linked to MCYST's phosphatase inhibition activity.
- Evidence of increased reactive oxygen species production and subsequent oxidative damage.
Conclusions:
- A single sublethal MCYST-LR dose induces significant renal alterations, including functional and structural damage.
- MCYST-LR impairs renal physiology by affecting glomerular filtration and sodium transport.
- The study underscores the nephrotoxic potential of MCYSTs even at sublethal doses, mediated by phosphatase inhibition and oxidative stress.
