Sunday 27 January 2013

Vectors of neurotoxin: Krill and the diatoms they eat


The diatom Pseudo-nitzschia australis produces the neurotoxin domoic acid (DA), which has been responsible for the death of many marine mammals and birds. The authors of this paper have outlined the need to study the organisms which can act as vectors for the DA through the trophic levels and have elected to study Krill as an attempt to quantify whether or not enough DA could pass through the food web in high enough levels to constitute a threat to marine mammals. The study assayed the homogenised samples of Krill in order to determine the toxicity levels and found that the toxin was only present in Euphausia pacifica when there were toxic Pseudo-nitzschia spp in the water column. This implies that the toxins in these Krill pass through the digestive tract of the Krill without being re-distributed throughout the rest of the body. However, this does not mean that the Krill are not effective vectors of DA as the levels of toxicity within the sampled individuals was measured to reach 44µg which far exceeds the acceptable human allowance for DA intake. This represents a problem for marine mammals which prey upon Krill, such as some cetaceans, which can ingest, in some cases, 2 tonnes of Krill at a time. The authors pointed out that although in some cases, ie whales, this may still not deliver a high enough dosage of DA to be harmful, however, during diving alot of the blood will flow to the heart and brain, as per the mammalian diving adaptations. This will also deliver alot of the toxin away from detoxification systems and directly into contact with the more important organs of the animal, which can most likely result in death. The resulting work of this paper highlights the need for further study into vectors of toxic algae during bloom times as this will allow for a greater understanding of the ecology of harmful algal blooms and the possible effects that they could have for marine mammals and birds in the future. 

Bargu S., Powell CL., Coale SL., Busman M., Doucette GJ., Silver MW., 2002, Krill: A potential vector for domoic acid in marine food webs, Marine Ecology Progress Series, 237, 209-216

4 comments:

  1. Hi Daniel,

    I posted a review of a paper earlier today suggesting that although domoic acid is present in increasing concentrations through the tophic levels of members of the pelagic food web, this is not evident for species in the benthic food web. I thought this would be an interesting update to the situation considering this paper was published at a later date in 2008.

    Research suggests that the toxin must pass out of the digest tract and enter the rest of the body for negative effects to be exhibited, and it is safe when only passing through the digestive tract. You stated that "the toxins in these Krill pass through the digestive tract of the Krill without being re-distributed throughout the rest of the body". I was wondering what evidence there is for this?

    Also, I read that domoic acid interferes with the ionotropic glutamate receptors, resulting in abnormal stimulation of nervous system. (Watanabe et al, 2011) Other interactions include induce free radical generation and dysfunction of mitochondria within the brain (Lu et al, 2012; Reiter et al, 2010) As you mentioned, once the toxin has entered the blood it can potentially collect until the threshold level is reached. It would be interesting to know how long the interaction last for, or if the damage is permanent, in order to gauge a time from in which the toxin can build up over.

    Lu J, Wu DM, Zheng YL, Hu B, Cheng W, Zhang ZF. (2012) Purple sweet potato color attenuates domoic acid-induced cognitive deficits by promoting estrogen receptor-α-mediated mitochondrial biogenesis signaling in mice. Free Radic Biol Med. 52(3):646-59.

    Russel J. Reiter,* Lucien C. Manchester, and Dun-Xian Tan (2010) Neurotoxins: Free Radical Mechanisms and Melatonin Protection, Curr Neuropharmacol 8(3) 194–210.

    Watanabe KH, Andersen ME, Basu N, Carvan MJ 3rd, Crofton KM, King KA, Suñol C, Tiffany-Castiglioni E, Schultz IR (2008) Defining and modeling known adverse outcome pathways: Domoic acid and neuronal signaling as a case study. Environ Toxicol Chem. 30(1):9-21.

    ReplyDelete
  2. Hi Danny and Megan,

    I’ve read both your blogs, I find the metabolism of domoic acid really interesting, I'm particularly intrigued how a compound can be extremely harmful to some organisms and totally harmless to others. Apart from the bioactivation in the gut of krill, have either of you found any information on why some organisms can metabolise this toxin whilst others can’t? This is something we discussed briefly in the lecture and I would be really interested to follow it up.

    Thanks,
    Vicky

    ReplyDelete
  3. This comment has been removed by the author.

    ReplyDelete
  4. Hi Vicky,

    I’m not sure about how the metabolism of domoic acid varies, however your comment provoked some thoughts about how other microbes that colonise the gut of fish have an impact on the effect of pathogenic introductions to fish. For example, Enterococcus faecalis stimulates the immune system (Rolfe, 2000), which no doubt proves benefits in terms of defending against pathogenic invasion.

    Microbes have also been found to alter the gene expression of other microbes in the gut, and of the host, across many species, including mice, insects and vertebrates (Dalmasso et al, 2011). It would be interesting to see if the microbes in the gut of marine organisms could alter the pathogenic ability of Pseudo-nitzschia species, and indeed any other pathogenic bacteria, such as suppressing the expression of genes that lead to toxin production. Specific genes are required for intestinal colonization, and to allow the complex process required for the bacteria to pass from the digestive tract to the blood stream, a method based around binding to receptors leading to apical endocytosis (Valério et al, 2010). If other bacteria present in the gut possess the ability to modulate expression of genes required for the above then this could explain why the infection does not occur in fish.

    Research into probiotics (in essence, beneficial bacteria commonly used a feed additives) has suggested the effects of certain bacteria are only present when they are continuously introduced to fish: after 2 weeks the microbial conditions of the gut are presumed to have returned to their original state (Merrifield et al, 2010). This could explain why Pseudo-nitzschia leave through the gut so readily, as they commonly occur in ‘blooms’ in the papers commented on in these blogs, and are therefore not constantly present.

    This research does not focus on domoic acid specifically, but there is potential that the theories could also be applied.

    On a separate note, I came across research stating a link with microbes and diabetes (Musso et al, 2010), a disease that I thought was diet or genetic related. It just shows how great the influence of microbes is!

    I hope this inspires further thought on the matter!

    Megan

    .

    Dalmasso, G; Nguyen, H. T. T; Yan, Y; Laroui, H; Charania, M. A; Ayyadurai, S; Sitaraman, S. V; and Didier Merlin, D (2011) Microbiota Modulate Host Gene Expression via MicroRNAs PLOS ONE, 6(4):e19293.

    Merrifield, D. L; Arkadios Dimitroglou, A; Foey, A; Davies, S. J; Baker, R. T. M; Bøgwald, J; Castex, M; and Ringø, E (2010) The current status and future focus of probiotics and prebiotic applications for salmonids. Aquaculture 302(1):1-18

    Musso, G; Gambino, R; and Cassader, M (2010) Obesity, Diabetes, and Gut Microbiota: The hygiene hypothesis expanded? Diabetes Care. 33(10): 2277–2284.

    Valério,E; Chaves, S; and Tenreiro, R; (2010) Diversity and Impact of Prokaryotic Toxins on Aquatic Environments: A Review, Toxins (Basel). 2(10): 2359–2410


    ReplyDelete

Note: only a member of this blog may post a comment.