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Natural Product Discovery with LC-MS/MS Diagnostic Fragmentation Filtering: Application for Microcystin Analysis
Published on: May 31, 2019
[Sub-acute hepatotoxicity of low doses of microcystins]
Wei Shi1, Huigang Zhu, Xiaorong Yan
1School of Public Health, Fudan University, Shanghai 200032, China.
Abstract:
In order to study sub-acute hepatotoxicity of low doses of microcystins in vivo, as well as to understand the mechanisms of hepatotoxicity of microcystins, eighty Spague-Dawley rats were injected with microcystins intraperitoneally at the doses of 0, 4, 8 and 12 micrograms.(kg.d)-1, respectively, for 35 days. Then blood and liver samples were used for assay. Several enzymatic levels and pathological changes were detected. Both terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and immunohistochemical methods were employed to study the apoptosis and proliferating cell nuclear antigen (PCNA). It was shown that the activity of serum gamma-glutamyltransferase (GGT) and concentrations of whole blood glutathione (GSH) decreased, serum activities of lactate dehydrogenase (LDH) and aminotransferase (AST) increased after exposure to MC. No significant change of concentration of serum alanine aminotransferase (ALT) was observed in the tested groups. Characteristic morphological alterations and active proliferation as well as apoptosis of hepatotocytes were observed in the treated groups. It was suggested that oxidative injury and apoptosis of hepatocytes induced by microcystins may be the mechanisms of its hepatotoxicity.
Insights
This study reveals that low-dose microcystin exposure in rats causes liver damage, indicated by altered enzyme levels and cellular changes. Oxidative stress and hepatocyte apoptosis are key mechanisms driving microcystin-induced hepatotoxicity.
Area of Science:
- Environmental toxicology
- Hepatology
- Biochemistry
Background:
- Microcystins (MCs) are potent cyanotoxins with known hepatotoxic effects.
- Understanding the sub-acute effects and mechanisms of low-dose MC exposure is crucial for risk assessment.
Purpose of the Study:
- To investigate the sub-acute hepatotoxicity of low-dose microcystins in vivo.
- To elucidate the underlying mechanisms of microcystin-induced liver injury.
Main Methods:
- Eighty Sprague-Dawley rats were administered varying doses of microcystins (0, 4, 8, 12 µg/kg/day) for 35 days.
- Blood and liver samples were analyzed for enzymatic levels (GGT, LDH, AST, ALT) and glutathione (GSH) concentrations.
- Apoptosis and cell proliferation were assessed using TUNEL and PCNA immunohistochemistry.
Main Results:
- Microcystin exposure led to decreased serum gamma-glutamyltransferase (GGT) and whole blood glutathione (GSH) levels.
- Increased serum lactate dehydrogenase (LDH) and aminotransferase (AST) activities were observed.
- Hepatocytes exhibited morphological alterations, increased proliferation, and apoptosis.
Conclusions:
- Low-dose microcystin exposure induces sub-acute hepatotoxicity in rats.
- Oxidative injury and apoptosis of hepatocytes are suggested as primary mechanisms of microcystin hepatotoxicity.
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