Journal
TOXINS
Volume 13, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/toxins13070506
Keywords
allelopathy; apoptosis; caspase-3; harmful algae; reactive oxygen species
Categories
Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACyT) [SAPPI 2021-0126, SIP 202111740, A1-S-14968]
- CONACyT [720383, BEIFI-2989]
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Allelopathy between phytoplankton species can promote cellular stress and programmed cell death, as shown by the effects of Chattonella marina var. marina, Margalefidinium polykrikoides, and Gymnodinium impudicum on Gymnodinium catenatum. Different species of phytoplankton induced varying levels of cellular stress and activation of programmed cell death markers in G. catenatum.
Allelopathy between phytoplankton species can promote cellular stress and programmed cell death (PCD). The raphidophyte Chattonella marina var. marina, and the dinoflagellates Margalefidinium polykrikoides and Gymnodinium impudicum have allelopathic effects on Gymnodinium catenatum; however, the physiological mechanisms are unknown. We evaluated whether the allelopathic effect promotes cellular stress and activates PCD in G. catenatum. Cultures of G. catenatum were exposed to cell-free media of C. marina var. marina, M. polykrikoides and G. impudicum. The mortality, superoxide radical (O-2(?-)) production, thiobarbituric acid reactive substances (TBARS) levels, superoxide dismutase (SOD) activity, protein content, and caspase-3 activity were quantified. Mortality (between 57 and 79%) was registered in G. catenatum after exposure to cell-free media of the three species. The maximal O-2(?-) production occurred with C. marina var. marina cell-free media. The highest TBARS levels and SOD activity in G. catenatum were recorded with cell-free media from G. impudicum. The highest protein content was recorded with cell-free media from M. polykrikoides. All cell-free media caused an increase in the activity of caspase-3. These results indicate that the allelopathic effect in G. catenatum promotes cell stress and caspase-3 activation, as a signal for the induction of programmed cell death.
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