Aedes aegypti mosquitoes, responsible for transmitting diseases such as dengue, Zika or yellow fever, are showing the first signs of resistance to alpha-cypermethrin, an insecticide from the pyrethroid family used to control populations of these insects. Now, a study has identified one of the main mechanisms that allow these living beings to defend themselves against the chemical compound: the activation of enzymes capable of detoxifying their body. The research, published in the scientific journal Frontiers in Tropical Diseases and carried out by scientists at the University of Delhi, in India, has analyzed how Aedes aegypti responds when exposed to alpha-cypermethrin. To do this, they exposed adult female mosquitoes to different concentrations of the product and found that, at the recommended diagnostic dose - 10 micrograms per bottle - 97.91% of the specimens died. According to the criteria used by the World Health Organization (WHO), this percentage points to a possible early appearance of resistance to the insecticide. The result shows that the repeated use of insecticides puts pressure on mosquito populations: those specimens that have mechanisms that allow them to tolerate the product better have a greater chance of surviving and transmitting those characteristics to subsequent generations. To understand how mosquitoes begin to protect themselves against the insecticide, the scientists studied five enzymes related to detoxification processes: beta-esterase, alpha-esterase, cytochrome P450, glutathione S-transferase (GST) and acetylcholinesterase (AChE). These proteins are part of the natural systems that insects have to deal with toxic substances and, when an insecticide enters the mosquito's body, some of these enzymes can intervene to transform or degrade its molecules and convert them into less harmful compounds that can then be eliminated. Computer molecular interaction analyzes showed that beta-esterase was the enzyme with the highest binding affinity for alpha-cypermethrin. This was followed by cytochrome, GST, alpha-esterase and acetylcholinesterase. Subsequent biochemical analyzes supported these results: the activity of several of these enzymes increased after exposure to the insecticide and the greatest effect was recorded precisely in beta-esterase, whose activity increased by 21.4%. A problem for disease control "Our study is valuable because it goes beyond demonstrating that resistance exists; it helps explain how it develops at the molecular level," says the lead author of the work, Sarita Kumar, professor at the Department of Zoology at the University of Delhi. Thus, researchers warn that knowing these mechanisms in an initial phase can be key to preventing resistance from spreading until certain products lose a good part of their effectiveness. Resistance to insecticides is one of the major problems for the control of diseases transmitted by mosquitoes. Aedes aegypti is one of the main vectors of several arboviruses and the use of chemicals continues to be an important tool to limit their populations, especially during epidemic outbreaks. However, its repeated or indiscriminate use favors the emergence of populations capable of surviving substances that were previously lethal. Hence, the authors emphasize the need to periodically monitor the sensitivity of mosquitoes and combine insecticides with other strategies, such as the elimination of places where they reproduce or biological control methods. "It is essential that this resistance is not yet widespread," highlights Kumar, who believes that the results offer an opportunity for health authorities to adopt management strategies. The scientists introduce, however, an important caution: the experiments were carried out with a laboratory-bred population, so resistance levels may vary between populations, geographical regions and natural conditions.
