Antioxidant enzymes form the first line of defense against free radicals in organisms. Their regulation depends mainly on the oxidant status of the cell, given that oxidants are their principal modulators. However, other factors have been reported to increase antioxidant enzyme activity and/or gene expression. During the last decade, the antioxidant melatonin has been shown to possess genomic actions, regulating the expression of several genes. Melatonin also influences both antioxidant enzyme activity and cellular mRNA levels for these enzymes. In the present report, we review the studies which document the influence of melatonin on the activity and expression of the antioxidative enzymes glutathione peroxidase, superoxide dismutases and catalase both under physiological and under conditions of elevated oxidative stress. We also analyze the possible mechanisms by which melatonin regulates these enzymes.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1600-079X.2003.00092.x

Regulation of antioxidant enzymes: a significant role for melatonin.

Introduction. Aluminium and zinc phosphides are highly effective insecticides and rodenticides and are used widely to protect grain in stores and during its transportation. Acute poisoning with these compounds may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine generated during their approved use. Mechanisms of toxicity. Both forms of poisoning are mediated by phosphine which has been thought to be toxic because it inhibits cytochrome c oxidase. While phosphine does inhibit cytochrome C oxidase in vitro, the inhibition is much less in vivo. It has been shown recently in nematodes that phosphine rapidly perturbs mitochondrial morphology, inhibits oxidative respiration by 70%, and causes a severe drop in mitochondrial membrane potential. This failure of cellular respiration is likely to be due to a mechanism other than inhibition of cytochrome C oxidase. In addition, phosphine and hydrogen peroxide can interact to form the highly reactive hydroxyl radical and phos...

Aluminium and zinc phosphide poisoning.

Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specific therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fluid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.

A Systematic Review of Aluminium Phosphide Poisoning

Fumigation with phosphine gas is by far the most widely used treatment for the protection of stored grain against insect pests. The development of high-level resistance in insects now threatens its continued use. As there is no suitable chemical to replace phosphine, it is essential to understand the mechanisms of phosphine toxicity to increase the effectiveness of resistance management. Because phosphine is such a simple molecule (PH3), the chemistry of phosphorus is central to its toxicity. The elements above and below phosphorus in the periodic table are nitrogen (N) and arsenic (As), which also produce toxic hydrides, namely, NH3 and AsH3. The three hydrides cause related symptoms and similar changes to cellular and organismal physiology, including disruption of the sympathetic nervous system, suppressed energy metabolism and toxic changes to the redox state of the cell. We propose that these three effects are interdependent contributors to phosphine toxicity.

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Mechanisms of Phosphine Toxicity

Development of resistance in major grain insect pest species to the key fumigant phosphine (hydrogen phosphide) across the globe has put the viability and sustainability of phosphine in jeopardy. The resistance problem has been aggravated over the past two decades, due mostly to the lack of suitable alternatives matching the major attributes of phosphine, including its low price, ease of application, proven effectiveness against a broad pest spectrum, compatibility with most storage conditions, and international acceptance as a residue-free treatment. In this review, we critically analyze the published literature in the area of phosphine resistance with special emphasis on the methods available for detection of resistance, the genetic basis of resistance development, key management strategies, and research gaps that need to be addressed.

Chiou Jong Chen

Papers

Phosphine-induced oxidative damage in rats: role of glutathione