Sharks are among some of the most amazing creatures in the world, and unfortunately some of the most threatened. They have flourished and remained virtually unchanged for hundreds of millions of years, until humans have begun overfishing them. The most tragic acts of over fishing are due to shark finning. Shark finning is the horrific catching of sharks, cutting off only their fins, throwing the rest of the shark back into the ocean, and left to die. This is beyond inhuman and has lead to the tragic decline of numerous shark species. There are various reasons to stop shark finning besides the pressing conservation issue. For example, many food critiques say that there is no actual taste to the shark fin, that it only adds texture. Some claim that the shark fin has natural holistic healing power. However, testing of the shark fins show that there is virtually no nutritional value to the shark fin. In addition, some research shows that these shark fins can also accumulate toxins.
One of these toxins is the potent cyanobacterial neurotoxin β-N-methylamino-L-alanine (BMAA). Researchers in this study have showed that there are dangerous levels of the BMAA toxin in 6/7 different shark species that were tested off the coast of Florida. There was some question after my presentation if the BMAA toxin actually has negative effects of humans or not. Therefore, I looked into some other primary resource studies to investigate. One interesting study I found looked into the exact actions of BMAA in the brain to see if there actually are negative neurological effects. However, this study was done in rats and not humans due to the ethical implications of a study like this on humans. Researchers found that the BMAA toxin inhibits a system called Xc- mediated cystine glutamate antiporter. In addition, when this Xc- system is inhibited it leads to low cell glutathione levels, which causes high oxidative stress and can lead to neurological damage and cell death. Glutathione is produced by a complex pathway in which cystine is taken up into the astrocytes and made into glutathione. According to this study, it was not known if BMAA inhibits cystine uptake into neurons or if it inhibits cystine into the astrocytes to prevent the release of glutathione. The data in this study strongly suggests BMAA inhibits cystine uptake, but also promotes the release of glutamate, which causes neural death by acting on receptors called mGluR5. This paper also sited some other papers that have done precedential work on BMAA’s affects on the brain. Studies have prove that inhabitation of the cystine uptake via Xc- mediated system can cause neural death and also shows that glutamate can kill cortical neurons. In addition, BMAA is proven to kill cerebellar granule cells. The toxin can accumulate in the cells and actually be permanently incorporated into the cells and cause misfolding of proteins. Thus, causing the neurodegenerative diseases. I think it would be interesting to see if there could be other studies to test the effects on humans instead of just extrapolating from lab animals. Such as on a cadaver brain, if that would even show any results on dead tissue or not? I am not sure if release of cystine or other pathways could still be detected in dead tissue.