Inspired by table salt – cyanide poisoning

Hi Readers,

I was eating my dinner early this week and I noticed on the salt bottle that an anticaking agent called ‘potassium ferrocyanide’ was used. I began to wonder, as I remembered learning in biology that cyanide is a competitive inhibitor, what the “ferro-” prefix signified and how the “ferro-” prevents it from inhibiting our enzymes.

After carrying out some online research I found that the ferrocyanide has its cyanide ions very tightly bound to the iron atom and stays with the iron right through the digestive system. The ferrocyanide cannot freely pass through the plasma membrane.

Nitrites can be used to treat for cyanide poisoning. The nitrites oxidise some of the haemoglobin’s iron converting the haemoglobin into methemoglobin. This releases more cytochrome oxidase enzyme (more of the enzyme which is being inhibited by the cyanide, which is preventing cellular respiration).

Cyanide binds to methemoglobin, forming cyanmethemoglobin. Treatment with nitrites is not really safe as methemoglobin cannot carry oxygen, and severe methemoglobinemia may occur and needs to be treated in turn with methylene blue (which used to be used to directly treat cyanide poisoning). Sodium nitrite is rapidly effective but can cause life-threatening toxicity (methemoglobinemia), whereas sodium thiosulfate – which can also be used to treat cyanide poisoning – has a delayed effect but is far safer.

I decided to look into cyanide poisoning in cattle, and the most frequent cause of acute and chronic cyanide poisoning in livestock is ingestion of plants that either contain cyanogenic glycosides (young plants, new shoots, and regrowth of plants after cutting often contain the highest levels of cyanogenic glycosides) or are induced to produce cyanogenic glycosides and cyanolipids.

Treatment

The affected cattle should be treated immediately by drenching with sodium thiosulphate. 60 g should be given in 600 ml of water. This can then be repeated hourly until the animal recovers.

The most effective treatment for cyanide poisoning is an intravenous injection of sodium thiosulphate. This is best administered by a vet at a dose rate of 660 mg/kg as well as oral/intraruminal doses of 30 g in 100 ml of water. The animals may require repeated intravenous doses if they relapse.

Sodium thiosulphate in a high dose can be effective when given up to 30 minutes after the ingestion of a toxic dose of cyanide, but it must be given as soon as possible.

Symptoms may include:

  • rapid laboured breathing
  • irregular pulse
  • frothing at the mouth
  • dilated pupils
  • muscle tremors
  • staggering

The mucous membranes are bright red in colour due to oxygen saturation of the haemoglobin.

If large quantities of cyanide are absorbed rapidly enough, the animals detoxification mechanisms will be overwhelmed and the animal will soon die. Affected animals rarely survive more than 1-2 hours after consuming the lethal quantities of cyanogenic plants and usually die within 5-15 minutes of developing clinical signs of poisoning.

Again, as I regularly mention, PREVENTION IS BETTER THAN A CURE! In order to prevent possible cyanide poisoning:

  • Graze sorghum, sorghum crosses, or john-songrass plants only when they are at least 18-24 inches tall.
  • Do not graze plants during drought periods when growth is severely reduced or the plant is wilted or twisted.  Slowed growth and the inability of the plant to maturefavours the formation of cyanogenic compounds in the leaves.
  • Do not graze potentially hazardous forages when frost is likely (including at night). Frost allows conversion to hydrogen cyanide within the plant. It is best not to allow ruminants to graze after a light frost as this is an extremely dangerous time and it may be several weeks before the cyanide potential subsides.
  • Do not allow access to wild cherry leaves.

Have any of you ever seen this in real life? I look forward to hearing any thoughts!

Sol

References

https://en.wikipedia.org/wiki/Ferrocyanide

https://www.quora.com/How-dangerous-is-E536-anti-caking-agent-potassium-ferrocyanide-on-salt

http://emedicine.medscape.com/article/814287-treatment https://www.daf.qld.gov.au/animal-industries/animal-health-and-diseases/protect-your-animals/poisonings-of-livestock/cyanide-and-nitrate-poisoning/treating-cyanide-and-nitrate-poisoning

http://www2.ca.uky.edu/agcomm/pubs/ID/ID220/ID220.pdf

“Fixing a broken heart”

Hi Readers,

Following a talk I recently had at school on UCAS applications as I start to think about applying to university, an interesting point was raised as a side topic by our guest speaker. He mentioned that zebrafish, a fish of no economic value to commercial fisheries, might help to extend our generations’ lifetime by almost 20 years.

The zebrafish is a special animal to biologists because its body is transparent. Therefore zebrafish are transparent early in their life cycle, so it is easy for researchers to see their hearts and blood vessels grow. Their hearts begin to develop after just 12 hours, and they reach adult size – about 3cm long – in about three months. They can provide research results barely three days later. If researchers modify the fish’s genotype at the egg stage, they can see a change in organ shape or dynamics very quickly.

In this 30-hour-old zebrafish embryo, you can observe developing organs like the retina (R), the brain (B), spinal chord (SC), the muscle (M) and the heart (H).

Heart tissue damage may occur when a person has suffered from a heart attack which affects their quality of life. Understanding what proteins allow human heart cells to multiply and regenerate, as they do in these fish, could help develop drugs that help our hearts to heal themselves.

If a person has a heart attack, the heart tissue lacks blood and therefore oxygen, causing it to become damaged or dead. Zebrafish can repair their hearts, unlike humans – heart muscle cells near the damaged area lose their muscle properties and revert back to stem cells. Scientists know that a protein called Mef2 is needed to turn zebrafish stem cells into heart muscle cells.

Dr Yaniv Hinits and colleagues believe that zebrafish muscle cells near wounds are able to turn Mef2 on and off – turning Mef2 off to revert to stem cells, before growing and turning Mef2 back on to repair the heart. Their team has been awarded a grant to find out if controlling Mef2could be used to treat damaged human heart tissue. They will study Mef2 in detail, find out if it can heal the heart after injury, and test if other proteins thought to influence recovery after heart attack are working through Mef2.

From my understanding, the grant was for three years and started 1st July 2014. I hope we hear some results in a few months time from this promising experiment.

Sol

https://www.bhf.org.uk/get-involved/mending-broken-hearts/research/zebrafish—do-they-hold-the-secret-cure

https://www.sciencedaily.com/terms/danio_rerio.htm

http://www.giraldezlab.org/Zebrafish.html