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Sulforaphane prevents microcystin-LR-induced oxidative damage and apoptosis in BALB/c mice
Xiaoyun Sun1, Lixin Mi, Jin Liu
1State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, CAS, People's Republic of China.
Abstract:
Microcystins (MCs), the products of blooming algae Microcystis, are waterborne environmental toxins that have been implicated in the development of liver cancer, necrosis, and even fatal intrahepatic bleeding. Alternative protective approaches in addition to complete removal of MCs in drinking water are urgently needed. In our previous work, we found that sulforaphane (SFN) protects against microcystin-LR (MC-LR)-induced cytotoxicity by activating the NF-E2-related factor 2 (Nrf2)-mediated defensive response in human hepatoma (HepG2) and NIH 3T3 cells. The purpose of this study was to investigate and confirm efficacy the SFN-induced multi-mechanistic defense system against MC-induced hepatotoxicity in an animal model. We report that SFN protected against MC-LR-induced liver damage and animal death at a nontoxic and physiologically relevant dose in BALB/c mice. The protection by SFN included activities of anti-cytochrome P450 induction, anti-oxidation, anti-inflammation, and anti-apoptosis. Our results suggest that SFN may protect mice against MC-induced hepatotoxicity. This raises the possibility of a similar protective effect in human populations, particularly in developing countries where freshwaters are polluted by blooming algae.
Insights
Sulforaphane (SFN) protects mice from liver damage caused by toxic Microcystins (MCs). This natural compound activates protective mechanisms, offering a potential strategy against algae-related toxins in drinking water.
Area of Science:
- Environmental Toxicology
- Hepatoprotective Agents
- Natural Product Chemistry
Background:
- Microcystins (MCs) are potent liver toxins produced by cyanobacteria blooms, posing risks to human health through contaminated water.
- Existing methods for MC removal are insufficient, necessitating alternative protective strategies against MC-induced hepatotoxicity.
- Previous research indicated sulforaphane (SFN) activates Nrf2-mediated defenses against MC-LR in cell lines.
Purpose of the Study:
- To investigate and confirm the efficacy of SFN's multi-mechanistic defense system against MC-induced hepatotoxicity in an animal model.
- To evaluate SFN's protective effects against MC-LR-induced liver damage and mortality in vivo.
- To elucidate the specific protective mechanisms of SFN, including anti-cytochrome P450 induction, anti-oxidation, anti-inflammation, and anti-apoptosis.
Main Methods:
- Administration of SFN at a nontoxic, physiologically relevant dose to BALB/c mice.
- Exposure of mice to microcystin-LR (MC-LR) to induce hepatotoxicity.
- Assessment of liver damage, animal survival rates, and key biochemical markers related to oxidative stress, inflammation, and apoptosis.
Main Results:
- SFN significantly protected BALB/c mice against MC-LR-induced liver damage and mortality.
- SFN demonstrated potent anti-cytochrome P450 induction, anti-oxidative, anti-inflammatory, and anti-apoptotic activities in vivo.
- The protective effects were observed at a safe and relevant dosage of SFN.
Conclusions:
- SFN confers significant protection against MC-induced hepatotoxicity in a mouse model.
- SFN's multi-mechanistic defense system offers a promising therapeutic or preventative approach against MCs.
- These findings suggest SFN's potential application for human populations exposed to MC-contaminated water, especially in developing regions.