Microcystin-LR induces alterations in heart muscle
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Published on: May 16, 2020
A Milutinović1, R Zorc-Pleskovic, D Petrovic
1Institute of Histology and Embryology, Medical School, Medical Faculty of Ljubljana, University of Ljubljana, Ljubljana, Slovenia. sandramilutinovic@yahoo.com
Abstract:
MC-LR belongs to a family of cyanobacterial toxins. MC-LR acts as serine-threonine phosphatase-1 and -2A inhibitor. Chronic intoxication with low doses of this toxin promotes liver tumour formation and induces kidney injury. The aim of the study was to evaluate whether chronic exposure to relatively low doses of MC-LR has toxic effects on hearts of treated animals. Male adult Wistar rats were treated every second day for 8 months with MC-LR (10microg/kg i. p., N = 5). Control groups were treated either with a vehicle (ethanol and methanol 4 : 1 v/v; N = 5) or with physiologic saline (N = 4). We found that MC-LR could induce enlargement of cardiomyocytes (MC-LR = 20.984microm+/-1.351, vehicle=17.454microm +/-0.518, saline = 15.996microm+/-1.430), loss of cell cross-striations, lower myofibril volume fraction (MC-LR = 0.3657mm(3)/mm(3) +/- 0.0337, vehicle=0.4716mm(3)/mm(3) +/-0.0086, saline = 0.4793 mm(3)/mm(3)+/-0.0101), fibrosis (MC-LR = 0.0747mm(3)/mm(3)+/-0.01288, vehicle = 0.0275 mm(3)/mm(3) +/- 0.0076, saline = 0.0309mm(3)/mm(3) +/-0.0074) and mononuclear infiltration in the interstitial tissue. The TUNEL staining of the heart sections of rats in all groups showed no apoptotic cells. We may conclude that long-term exposure to relatively low doses of MC-LR represents a considerable risk of injury of the heart.
Insights
Chronic exposure to microcystin-LR (MC-LR), a cyanobacterial toxin, causes significant heart damage in rats. This study reveals MC-LR induces cardiac hypertrophy and fibrosis, posing a risk to heart health even at low doses.
Area of Science:
- Environmental Toxicology
- Cardiovascular Pathology
- Cyanobacterial Toxin Research
Background:
- Microcystin-LR (MC-LR) is a potent cyanobacterial toxin known to cause liver and kidney damage.
- Previous research indicates MC-LR's role in promoting liver tumors and kidney injury with chronic low-dose exposure.
- The cardiotoxic effects of long-term, low-dose MC-LR exposure remain incompletely understood.
Purpose of the Study:
- To investigate the potential cardiotoxic effects of chronic, low-dose exposure to MC-LR in a rodent model.
- To evaluate structural and cellular changes in the heart following prolonged MC-LR administration.
Main Methods:
- Adult male Wistar rats were administered MC-LR (10 µg/kg) every other day for 8 months.
- Control groups received either a vehicle solution or physiologic saline.
- Cardiac tissue was analyzed for cardiomyocyte size, myofibril volume, fibrosis, and inflammatory cell infiltration.
Main Results:
- MC-LR exposure led to significant cardiomyocyte enlargement compared to control groups.
- A reduction in myofibril volume fraction and an increase in cardiac fibrosis were observed in MC-LR-treated rats.
- Mononuclear cell infiltration in the interstitial tissue and loss of cardiomyocyte cross-striations were noted, without evidence of apoptosis.
Conclusions:
- Chronic exposure to low doses of MC-LR induces significant cardiac injury in rats.
- Observed effects include cardiac hypertrophy, fibrosis, and inflammation, indicating a substantial risk to heart health.
- MC-LR should be considered a potential cardiotoxin, necessitating further investigation into its mechanisms and human health implications.
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