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Daily News Blog

30
Sep

Neonicotinoid Insecticides Trigger Neurodegeneration and Can Blind Insects at Low Doses

(Beyond Pesticides, September 30, 2020) Low doses of neonicotinoid (neonic) insecticides are known to disrupt insect learning and behavior, but new science is providing a better understanding of how these effects manifest at a cellular level. Published in the Proceedings of the National Academy of Sciences, this study finds that the neonic imidacloprid binds to brain receptors, triggering oxidative stress, reducing energy levels, and causing neurodegeneration.

“Although many studies have shown that low doses of insecticides can affect insect behavior, they have not uncovered whether insecticides trigger changes at the cellular and molecular levels,” said lead author Felipe Martelli, PhD, of Monash University in Melbourne, Australia. “The goal of this work was to have a better understanding of the effects of low doses of the common insecticide imidacloprid at the cellular, physiological and behavioral levels.”

Researchers used the fruit fly Drosophilia melanogaster, a common experimental organism, as it contains a number of nicotinic acetylchloline receptors, the primary site of action for imidaclorpid. The neonic binds to these receptors, which regulate a number of physiological processes, such muscle contraction. Binding closes these channels, leading to the range of harm researchers observed through their study.

Larval fuit flies were exposed to imidacloprid for two hours at 2.5 parts per million (ppm), less than 3% of the application rate insects are likely to encounter in the field. At this rate, test-reared flies display reduced movement, but do not die. However, scientific observation found that, although the flies are not dying, the neonic exposure induce a sequence of compounding negative health effects.

“We discovered that imidacloprid did bind to the nicotinic receptors in the larvae’s nervous system, causing a long, enduring influx of calcium ions into the neurons. Having too much calcium inside the neurons damaged the mitochondria, the energy-producing structures of the cell. This led to the accumulation of significant amounts of reactive oxygen species (ROS), or free radicals inside the brain that triggered a cascade of damaging events that spread to many other tissues,” Dr. Martelli said.

ROS leads to an imbalance in the development of lipid droplets throughout the fly’s organ systems. “Lipids are much more than energy storage. They play many important roles in the body, from being a crucial part of the integrity of cell membranes to working as messenger molecules or in hormone synthesis,” said Phillip Battenham, PhD, of the University of Melbourne. “In addition to lipid alterations, we also observed that imidacloprid triggered changes in the activity of genes related to metabolism, energy production, detoxification and the immune response. The overall physiology of the larvae was systemically impaired.”

Scientists were able to confirm that imidacloprid is causing these impacts by successfully treating some larvae with an antioxidant known to mediate the effects being observed.

Harmful effects are also seen in adult fruit flies exposed to the neonic. A dose of 4 ppm, known to cause death in 50% of exposed flies within a month, was used, and researchers observed the flies for the first 10 days of exposure. Dosed flies performed poorly on tests assessing their climbing ability and recovery after disturbance – indications of neurodegeneration. Vision was significantly impacted, with damage to mitochontrial photoreceptors effectively rendering the flies blind.

“When we looked closer at the light-sensing cells in the adult fly’s retina, we found that glial cells, which provide support and protection to neurons, had progressively accumulated vacuoles and a significant number of defective mitochondria, indications that the glia were dying,” said Hugo Bellen, PhD, of Baylor University and Texas Children’s Hospital.

As with the larva, an antioxidant treatment was able to decrease the extent of damage caused by imidacloprid exposure. “It is concerning that even at low doses, insecticides can cause neurological damage, disrupt energy production and compromise the immune system of insects,” Dr. Batterham said. “Those problems can make it more challenging for insects to adapt to other stresses, such as climate change or infections. Our findings emphasize the importance of better understanding the mechanisms of action of insecticides, in particular on beneficial insects.”

Pollinators are perhaps the most well known victim of exposure to systemic neonicotinoid insecticides, but as the global Task Force on Systemic Insecticides shows the entire invertebrate world, and therefore the ecosystems that depend upon them, is at risk. Further evidence finds these chemicals are directly harming a range of other life, including amphibians, birds, and mammals, including humans, as indirect effects move up the food chain.

It is not too late to intervene and stop the use of these harmful substances. Call your member of Congress and urge them to cosponsor the Saving America’s Pollinator Act, which would eliminate neonic use in the United States. Become active in your community and state by gathering together with like minded friends and neighbors, and reaching out to your elected officials about this issue. Get familiar with the science through Beyond Pesticides past daily news posts as well as the Bee Protective webpage.

All unattributed positions and opinions in this piece are those of Beyond Pesticides.

Source: PNAS, Baylor College of Medicine press release

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