‘Griffin

يعتبر السيانيد من أخطر المواد غير العضوية السامة للإنسان، إذ يمكن أن يؤدي إلى الموت خلال ثوان معدودة بسبب نقص الأكسدة الخلوية التي تصيب الخلايا.

يوجد السيانيد على شكل غاز هيدروجيني أو على شكل صلب. ويحتاج الإنسان إلى كمية لا تتجاوز 0.2 من الغرام حتى يلقى حتفه المباشر خلال ثوان. و يؤدي استنشاق السيانيد إلى تسمم الجسم عن طريق ايقاف عمليات الاكسدة الخلوية وموتها، قبل ذلك يعاني الإنسان من اعرض سريرية متعددة نذكر منها: الشعور بالدوخة والغثيان والتقيؤ وفقدان الوعي وبالنهاية توقف القلب والموت المفاجئ.

واشارت الدراسات الحديثة إلى أن استنشاق 200 إلى 500 جزء من هيدروجين السيانيد موجودة في مليون جزيء من الهواء لمدة 30 دقيقة، تؤدي إلى موت الإنسان.




Cyanide is generally considered to be a rare source of poisoning; however, cyanide exposure occurs relatively frequently in patients with smoke inhalation from residential or industrial fires. Cyanide poisoning also may occur in industry, particularly in the metal trades, mining, electroplating, jewelry manufacturing, and x-ray film recovery. It is also encountered in fumigation of ships, warehouses, and other structures. Cyanides are also used as suicidal agents, particularly among healthcare and laboratory workers, and they can potentially be used in a terrorist attack

Numerous forms of cyanide exist, including gaseous hydrogen cyanide (HCN), water-soluble potassium and sodium cyanide salts, and poorly water-soluble mercury, copper, gold, and silver cyanide salts. In addition, a number of cyanide-containing compounds, known as cyanogens, may release cyanide during metabolism. These include, but are not limited to, cyanogen chloride and cyanogen bromide (gases with potent pulmonary irritant effects), nitriles (R-CN), and sodium nitroprusside, which may produce iatrogenic cyanide poisoning during prolonged or high-dose intravenous therapy (>10 mcg/kg/min)

Industry widely uses nitriles as solvents and in the manufacturing of plastics. Nitriles may release HCN during burning or when metabolized following absorption by the skin or gastrointestinal tract. A number of synthesized (eg, polyacrylonitrile, polyurethane, polyamide, urea-formaldehyde, melamine) and natural (eg, wool, silk) compounds produce HCN when burned. These combustion gases likely contribute to the morbidity and mortality from smoke inhalation

Finally, chronic consumption of cyanide-containing foods, such as cassava root or apricot seeds[1] , may lead to cyanide poisoning

Overall, depending on its form, cyanide may cause toxicity through parenteral administration, inhalation, ingestion, or dermal absorption.
Cyanide affects virtually all body tissues, attaching itself to ubiquitous metalloenzymes and rendering them inactive. Its principal toxicity results from inactivation of cytochrome oxidase (at cytochrome a3), thus uncoupling mitochondrial oxidative phosphorylation and inhibiting cellular respiration, even in the presence of adequate oxygen stores. Cellular metabolism shifts from aerobic to anaerobic, with the consequent production of lactic acid. Consequently, the tissues with the highest oxygen requirements (brain and heart) are the most profoundly affected by acute cyanide poisoning

Chronic consumption of cyanide-containing foods eventually can result in ataxia and optic neuropathy. Defective cyanide metabolism due to rhodanese deficiency may explain development of Leber optic atrophy, leading to subacute blindness. Cyanide also may cause some of the adverse effects associated with chronic smoking, such as tobacco amblyopia