Hydrogen sulfide (H₂S) remains a chemical hazard in the gas and farming industry. It is easy to manufacture from common chemicals and thus represents a potential threat for the civilian population. It is also employed as a method of suicide, for which incidence has recently increased in the US.

H₂S is a mitochondrial poison and exerts its toxicity through mechanisms that are thought to result from its high affinity to various metallo-proteins (such as – but not exclusively- the mitochondrial cytochrome c oxidase) and interactions with cysteine residues of proteins. Ion channels with critical implications for the cardiac and the brain functions appear to be affected very early during and following H₂S exposure, an effect which is rapidly reversible during a light intoxication. However, during severe H₂S intoxication, a coma, associated with a reduction in cardiac contractility, develops within minutes or even seconds leading to death by complete electro-mechanical dissociation of the heart. If the level of intoxication is milder, a rapid and spontaneous recovery of the coma occurs as soon as the exposure stops. The risk, although probably very small, of developing long-term debilitating motor or cognitive deficits is present. One of the major challenges impeding our effort to offer an effective treatment against H₂S intoxication after exposure is that the pool of free/soluble H₂S almost immediately disappears from the body preventing agents trapping free H₂S (cobalt or ferric compounds) to play their protective role.

This paper (1) presents and discusses the neurological symptoms and lesions observed in various animals models and in humans following an acute exposure to sub-lethal or lethal levels of H₂S, (2) reviews the potential interest of methylene blue (MB), a potent cyclic redox dye – currently used for the treatment of methemoglobinemia – which has potential rescuing effects on the mitochondrial activity, as an antidote against sulfide intoxication.

硫化氢（H ₂ S）在天然气和农业中仍然是化学危害。它很容易用普通化学品制造，因此对平民人口构成潜在威胁。它也被用作自杀方法，在美国，最近这种情况的发生率有所上升。

H ₂ S是线粒体毒物，并通过其机理发挥其毒性，该机理被认为是由其对各种金属蛋白（例如但不限于线粒体细胞色素c氧化酶）的高度亲和力以及与蛋白的半胱氨酸残基相互作用引起的。暴露于H ₂ S期间和之后，对心脏和大脑功能至关重要的离子通道似乎很早就受到了影响，这种影响在光中毒期间可以迅速逆转。但是，在重度H ₂期间S中毒是一种与心脏收缩力下降有关的昏迷，在几分钟甚至几秒钟内发展成心脏完全机电分离导致死亡。如果中毒程度较轻，则一旦停止接触，就会迅速而自然地恢复昏迷状态。尽管可能很小，但存在长期使人虚弱的运动或认知缺陷的风险。阻碍我们为暴露后的H ₂ S中毒提供有效治疗的主要挑战之一是，游离/可溶H ₂ S池几乎立即从体内捕获游离H ₂ S（钴或铁化合物）的预防剂中消失。发挥保护作用。

本文（1）提出并讨论了急性暴露于亚致命或致命水平的H ₂ S后在各种动物模型和人类中观察到的神经系统症状和病变，（2）综述了亚甲蓝（MB）的潜在用途，一种有效的环状氧化还原染料，目前用于治疗高铁血红蛋白血症，对线粒体活性具有潜在的挽救作用，可作为抗硫化物中毒的解毒剂。