User talk:Jitender Rathi

Jitender Rathi

science
Today now science is creating us God. Jitender Rathi (talk) 10:33, 3 March 2015 (UTC)

The chemistry of poison - Cyanide
The second in the series on poisons looks at cyanide, another notorious agent of murder. It’s played a role in genocide, in suicide pills, and is also found in small amounts in the seeds of numerous fruits. So, why is cyanide so poisonous, and why are deaths from cyanide poisoning less of a rarity than those from arsenic poison in the modern day?

Cyanide is the CN- ion, and as a poison it is commonly administered as one of the three compounds shown in the graphic: hydrogen cyanide, a volatile, colourless liquid, and potassium and sodium cyanide, both white powders. Both potassium and sodium cyanide react with stomach acid to produce hydrogen cyanide, which can then go on to cause toxic effects.

Though cyanide has been used as a poison for centuries, it was first isolated in Sweden in 1782, by Swedish chemist Carl Scheele. Whilst different sources tell different stories, some claim that the exposure to cyanide was a contributing cause to Scheele’s early death at the age of 43. Scheele’s early death isn’t surprising considering considering the number of toxic agents he worked with throughout his career. He was also the first person to note the bitter almond smell of hydrogen cyanide – a smell which, it turns out, can only be detected by 40% of people for genetic reasons.

So, what happens when a person is poisoned with cyanide? It’s one of the fastest acting poisons known, and if a significant amount is ingested, it can lead rapidly to death. Upon ingestion, it binds to haemoglobin, the molecule in red blood cells responsible for carrying oxygen to the cells in our body. Haemoglobin then ferries it to the body’s tissues, where it can bind to an enzyme called cytochrome oxidase. This enzyme is a vital tool cells require to make use of oxygen, and with cyanide bound to it, they are unable to do so.

The symptoms of cyanide exposure are seen rapidly, and include headaches, nausea, vomiting, and elevated breathing and heart rates. With a suitable dose, these symptoms can quickly progress to loss of consciousness, respiratory failure, and death. The exact dose that causes death depends on the form of cyanide administered, but lethal doses as low as one milligram per kilogram of body weight have been reported.

Cyanide poisoning can also come from unlikely sounding sources. One study tells of a woman who ate 20 apricot kernels, and was subsequently afflicted with cyanide poisoning. Apricot kernels, and seeds of other fruits such as apples and peaches, contain a compound called amygdalin, which contains a cyanide portion. When this compound contacts with the acid in the stomach, hydrogen cyanide is produced, which can then lead to poisoning. Luckily, a significant number of fruit seeds are required to reach a lethal dose of cyanide – the woman mentioned in the study made a full recovery.

Perhaps the most well-known use of cyanide as a poison was in the Nazi concentration camps of World War II. There, the Nazis used Zyklon B, a cyanide-based pesticide which released hydrogen cyanide, to kill millions. Cyanide was also involved later in the war; though it’s commonly thought that Hitler committed suicide by shooting himself in the head, evidence has suggested that he in fact killed himself via use of a pill containing potassium cyanide, along with his mistress Eva Braun.

Cyanide poisoning is still a not-uncommon occurrence, though the exposure is often accidental. In particular, plastics such as nylon and polyurethanes release cyanide when burnt, so during fires cyanide poisoning can often occur. In 2009, a Russian nightclub fire killed over 150 people, and a number of these deaths were thought to be as a result of the inhalation of cyanide and other toxic gases produced by burning plastics.

As cyanide is such a fast-acting poison, it can be hard to administer any antidote in time if a lethal dose has been ingested. There’s no universally agreed method for treating cyanide poisonings, and different treatments are favoured in differen Jitender Rathi (talk) 04:17, 4 March 2015 (UTC)

The chemistry of poison - Cyanide
The second in the series on poisons looks at cyanide, another notorious agent of murder. It’s played a role in genocide, in suicide pills, and is also found in small amounts in the seeds of numerous fruits. So, why is cyanide so poisonous, and why are deaths from cyanide poisoning less of a rarity than those from arsenic poison in the modern day?

Cyanide is the CN- ion, and as a poison it is commonly administered as one of the three compounds shown in the graphic: hydrogen cyanide, a volatile, colourless liquid, and potassium and sodium cyanide, both white powders. Both potassium and sodium cyanide react with stomach acid to produce hydrogen cyanide, which can then go on to cause toxic effects.

Though cyanide has been used as a poison for centuries, it was first isolated in Sweden in 1782, by Swedish chemist Carl Scheele. Whilst different sources tell different stories, some claim that the exposure to cyanide was a contributing cause to Scheele’s early death at the age of 43. Scheele’s early death isn’t surprising considering considering the number of toxic agents he worked with throughout his career. He was also the first person to note the bitter almond smell of hydrogen cyanide – a smell which, it turns out, can only be detected by 40% of people for genetic reasons.

So, what happens when a person is poisoned with cyanide? It’s one of the fastest acting poisons known, and if a significant amount is ingested, it can lead rapidly to death. Upon ingestion, it binds to haemoglobin, the molecule in red blood cells responsible for carrying oxygen to the cells in our body. Haemoglobin then ferries it to the body’s tissues, where it can bind to an enzyme called cytochrome oxidase. This enzyme is a vital tool cells require to make use of oxygen, and with cyanide bound to it, they are unable to do so.

The symptoms of cyanide exposure are seen rapidly, and include headaches, nausea, vomiting, and elevated breathing and heart rates. With a suitable dose, these symptoms can quickly progress to loss of consciousness, respiratory failure, and death. The exact dose that causes death depends on the form of cyanide administered, but lethal doses as low as one milligram per kilogram of body weight have been reported.

Cyanide poisoning can also come from unlikely sounding sources. One study tells of a woman who ate 20 apricot kernels, and was subsequently afflicted with cyanide poisoning. Apricot kernels, and seeds of other fruits such as apples and peaches, contain a compound called amygdalin, which contains a cyanide portion. When this compound contacts with the acid in the stomach, hydrogen cyanide is produced, which can then lead to poisoning. Luckily, a significant number of fruit seeds are required to reach a lethal dose of cyanide – the woman mentioned in the study made a full recovery.

Perhaps the most well-known use of cyanide as a poison was in the Nazi concentration camps of World War II. There, the Nazis used Zyklon B, a cyanide-based pesticide which released hydrogen cyanide, to kill millions. Cyanide was also involved later in the war; though it’s commonly thought that Hitler committed suicide by shooting himself in the head, evidence has suggested that he in fact killed himself via use of a pill containing potassium cyanide, along with his mistress Eva Braun.

Cyanide poisoning is still a not-uncommon occurrence, though the exposure is often accidental. In particular, plastics such as nylon and polyurethanes release cyanide when burnt, so during fires cyanide poisoning can often occur. In 2009, a Russian nightclub fire killed over 150 people, and a number of these deaths were thought to be as a result of the inhalation of cyanide and other toxic gases produced by burning plastics.

As cyanide is such a fast-acting poison, it can be hard to administer any antidote in time if a lethal dose has been ingested. There’s no universally agreed method for treating cyanide poisonings, and different treatments are favoured in differen Jitender Rathi (talk) 04:17, 4 March 2015 (UTC)