Sufonylurea pesticides are a class of very potent pesticides introduced and marketed heavily in the early 1980s. These include the herbicides Metsulfuron-methy, Diuron, Chlortoluron, Monolinuron, Tebuthiuron, Sulfometuron methyl

Amidazolinone pesticides are another class of very potent pesticides that include imazapyr, imazapic, imazamethabenz-methyl, imazethapyr, imazaquin, and imazamox.

On a molecular level, these herbicides inhibits the activity of an enzyme called acetolactate synthase(ALS). ALS is one of the enzymes used by plants to synthesize three specific amino acids, molecules that are used as components of proteins.

These herbicides are claimed to be safe based on the claim that mammals do not have the enzymes acteolactate synthase or acetohydroxyacid synthase. This is not true, an acteolactate synthase homolog has been found in Humans.

Additionally sulfonylureas have been used in diabetes medications, where they have been shown to induce hypoglycemia. Sulfonylureas inhibit ATP-sensitive potassium channels in pancreatic beta cells., which causes cell membrane depolarization, opening of voltage-dependent calcium channels, thus triggering an increase in intracellular calcium into the beta cell which stimulates insulin release.

Sulfonylureas are potentially teratogenic and cannot be used in pregnancy or in patients who may become pregnant. Sulfonylureas have been shown to increase death, and they interfere with estrogens, and thyroid hormones. They induce hypothyroidism, and congentital hypothyroidism could be considered a teratogenic affect.

The insecticide Dimilin (diflubenzuron) a chitin inhibitor, also has the same mode of action as the above herbicides.  It has been demonstrated that diflubenzuron is interchangeable with sulfonylurea diabetes medications, and that they have the same mode of action.

Implications of these bio-chemical interactions with regard to wildlife malformations and mineral deficiencies:

Copper deficiencies: Copper deficiencies are rare, but are known to be associated with disturbed carbohydrate metabolism. copper deficiencies have been prevalent among declining wildlife populations for at least the last 20 years. Sulfonylureas increase insulin production in the pancreas and alter carbohydrate metabolism via altered glucose utilization. Many (~10%) diabetes patients using sulfonylureas exhibit insulin “burn out” where insulin production is completely shut down. This is at low therapeutic does, if the case of large, unregulated doses, diabetes could theoretically be induced by similar pancreatic burn out.  Environmental diabetes has been implicated in copper deficient moose in Sweden.

Selenium deficiency: Coupled with copper deficiencies, selenium deficiencies occur simultaneously in declining wildlife populations. Like copper selenium has been shown to play a role in liver glucose regulation. High hepatic selenium levels have been associated with hyperglycemia.  Sulfonylureas induce hypoglycemia, and could in theory then induce low hepatic selenium levels. Animal studies suggest that selenium, particularly in combination with vitamin E, may lower blood sugar levels over time.

Laminitis: There is an association between insulin resistance and laminitis. Sulfonylureas have a direct affect on the pancrease, and insulin production.

Magnesium deficiencies: Wildlife in many parts of the West have been observed targeting magnesium chloride on the side of the road. Magnesium chloride is a soluble and available form of magnesium for these animals. Diabetes and other metabolic and endocrine disruptions induce magnesium deficiencies. To complicate matters, magnesium increases the absorption of sulfonylureas. There is a clear association between sulfonylureas and magnesium. When sulfonylureas attach to the enzyme acteolactate synthase, it affects the way in which magnesium(Mg2) is attached to the ALS enzyme.

Under bites: As mentioned above sulfonylureas have been shown to induce hypothyroidism. Under bites are symptomatic of congenital hypothyroidism. 

Testicular atrophy: Sulfonylureas have been shown to induce testicular atrophy in lab animals.

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