scholarly journals A Possible Link Between Pyriproxyfen and Microcephaly

2017 ◽  
Author(s):  
Yaneer Bar-Yam ◽  
H. Frederik Nijhout ◽  
Raphael Parens ◽  
Felipe Costa ◽  
Alfredo J. Morales
Keyword(s):  
Juvenile Hormone ◽  
Developmental Disorders ◽  
Molecular Mechanisms ◽  
Viral Infections ◽  
Developmental Toxicity ◽  
Causal Link ◽  
Cross Reactivity ◽  
Retinoid X Receptor ◽  
Juvenile Hormone Analog ◽  
Hormone Analog

The Zika virus has been the primary suspect in the large increase in incidence of microcephaly in 2015-6 in Brazil. However its role is not confirmed despite individual cases in which viral infections were found in neural tissue. Recently, the disparity between the incidences in different geographic locations has led to questions about the virus’s role. Here we consider the alternative possibility that the use of the insecticide pyriproxyfen for control of mosquito populations in Brazilian drinking water is the primary cause. Pyriproxifen is a juvenile hormone analog which has been shown to correspond in mammals to a number of fat soluble regulatory molecules including retinoic acid, a metabolite of vitamin A, with which it has cross-reactivity and whose application during development has been shown to cause microcephaly. Methoprene, another juvenile hormone analog that was approved as an insecticide based upon tests performed in the 1970s, has metabolites that bind to the mammalian retinoid X receptor, and has been shown to cause developmental disorders in mammals. Isotretinoin is another example of a retinoid causing microcephaly in human babies via maternal exposure and activation of the retinoid X receptor in developing fetuses. Moreover, tests of pyriproxyfen by the manufacturer, Sumitomo, widely quoted as giving no evidence for developmental toxicity, actually found some evidence for such an effect, including low brain mass and arhinencephaly—incomplete formation of the anterior cerebral hemispheres—in exposed rat pups. Finally, the pyriproxyfen use in Brazil is unprecedented— it has never before been applied to a water supply on such a scale. Claims that it is not being used in Recife, the epicenter of microcephaly cases, do not distinguish the metropolitan area of Recife, where it is widely used, and the municipality, and have not been adequately confirmed. Given this combination of information about molecular mechanisms and toxicological evidence, we strongly recommend that the use of pyriproxyfen in Brazil be suspended until the potential causal link to microcephaly is investigated further.

scholarly journals A Possible Link Between Pyriproxyfen and Microcephaly

2016 ◽  
Author(s):  
Dan Evans ◽  
Fred Nijhout ◽  
Raphael Parens ◽  
Alfredo J. Morales ◽  
Yaneer Bar-Yam
Keyword(s):  
Juvenile Hormone ◽  
Developmental Disorders ◽  
Viral Infections ◽  
Mosquito Control ◽  
Developmental Toxicity ◽  
Cross Reactivity ◽  
Retinoid X Receptor ◽  
Rat Pups ◽  
Juvenile Hormone Analog ◽  
Hormone Analog

The Zika virus is the primary suspect in the large increase in microcephaly cases in 2015-6 in Brazil, however its role is unconfirmed despite individual cases of viral infections found in neural tissue. Here we consider the alternative that the insecticide pyriproxyfen, used in Brazilian drinking water for mosquito control, may actually be the cause. Pyriproxifen is an analog of juvenile hormone, which corresponds in mammals to regulatory molecules including retinoic acid, a vitamin A metabolite, with which it has cross-reactivity and whose application during development causes microcephaly. Methoprene, another juvenile hormone analog approved as an insecticide has metabolites that bind to the retinoid X receptor, and causes developmental disorders in mammals. Isotretinoin is another example of a retinoid causing microcephaly in human babies via activation of the retinoid X receptor. Moreover, tests of pyriproxyfen by the manufacturer, Sumitomo, widely quoted as giving no evidence for developmental toxicity, actually found some evidence for such an effect, including low brain mass and arhinencephaly—incomplete formation of the anterior cerebral hemispheres—in rat pups. Finally, the pyriproxyfen use in Brazil is unprecedented—it has never before been applied to a water supply on such a scale. Claims that it is not being used in Recife, the epicenter of microcephaly cases, do not distinguish the metropolitan area of Recife, where it is widely used, and the municipality, where it is not. Given this combination of information we strongly recommend that the use of pyriproxyfen in Brazil be suspended pending further investigation.

scholarly journals A possible link between pyriproxyfen and microcephaly

2016 ◽  
Author(s):  
Dan Evans ◽  
Fred Nijhout ◽  
Raphael Parens ◽  
Alfredo J Morales ◽  
Yaneer Bar-Yam
Keyword(s):  
Juvenile Hormone ◽  
Developmental Disorders ◽  
Viral Infections ◽  
Mosquito Control ◽  
Developmental Toxicity ◽  
Cross Reactivity ◽  
Retinoid X Receptor ◽  
Rat Pups ◽  
Juvenile Hormone Analog ◽  
Hormone Analog

The Zika virus is the primary suspect in the large increase in microcephaly cases in 2015-6 in Brazil, however its role is unconfirmed despite individual cases of viral infections found in neural tissue. Here we consider the alternative that the insecticide pyriproxyfen, used in Brazilian drinking water for mosquito control, may actually be the cause. Pyriproxifen is an analog of juvenile hormone, which corresponds in mammals to regulatory molecules including retinoic acid, a vitamin A metabolite, with which it has cross-reactivity and whose application during development causes microcephaly. Methoprene, another juvenile hormone analog approved as an insecticide has metabolites that bind to the retinoid X receptor, and causes developmental disorders in mammals. Isotretinoin is another example of a retinoid causing microcephaly in human babies via activation of the retinoid X receptor. Moreover, tests of pyriproxyfen by the manufacturer, Sumitomo, widely quoted as giving no evidence for developmental toxicity, actually found some evidence for such an effect, including low brain mass and arhinencephaly--incomplete formation of the anterior cerebral hemispheres--in rat pups. Finally, the pyriproxyfen use in Brazil is unprecedented--it has never before been applied to a water supply on such a scale. Claims that it is not being used in Recife, the epicenter of microcephaly cases, do not distinguish the metropolitan area of Recife, where it is widely used, and the municipality, where it is not. Given this combination of information we strongly recommend that the use of pyriproxyfen in Brazil be suspended pending further investigation.

scholarly journals A possible link between pyriproxyfen and microcephaly

2016 ◽  
Author(s):  
Dan Evans ◽  
Fred Nijhout ◽  
Raphael Parens ◽  
Alfredo J Morales ◽  
Yaneer Bar-Yam
Keyword(s):  
Juvenile Hormone ◽  
Developmental Disorders ◽  
Viral Infections ◽  
Mosquito Control ◽  
Developmental Toxicity ◽  
Cross Reactivity ◽  
Retinoid X Receptor ◽  
Rat Pups ◽  
Juvenile Hormone Analog ◽  
Hormone Analog

The Zika virus is the primary suspect in the large increase in microcephaly cases in 2015-6 in Brazil, however its role is unconfirmed despite individual cases of viral infections found in neural tissue. Here we consider the alternative that the insecticide pyriproxyfen, used in Brazilian drinking water for mosquito control, may actually be the cause. Pyriproxifen is an analog of juvenile hormone, which corresponds in mammals to regulatory molecules including retinoic acid, a vitamin A metabolite, with which it has cross-reactivity and whose application during development causes microcephaly. Methoprene, another juvenile hormone analog approved as an insecticide has metabolites that bind to the retinoid X receptor, and causes developmental disorders in mammals. Isotretinoin is another example of a retinoid causing microcephaly in human babies via activation of the retinoid X receptor. Moreover, tests of pyriproxyfen by the manufacturer, Sumitomo, widely quoted as giving no evidence for developmental toxicity, actually found some evidence for such an effect, including low brain mass and arhinencephaly--incomplete formation of the anterior cerebral hemispheres--in rat pups. Finally, the pyriproxyfen use in Brazil is unprecedented--it has never before been applied to a water supply on such a scale. Claims that it is not being used in Recife, the epicenter of microcephaly cases, do not distinguish the metropolitan area of Recife, where it is widely used, and the municipality, where it is not. Given this combination of information we strongly recommend that the use of pyriproxyfen in Brazil be suspended pending further investigation.

EFFECTS OF ECDYSONES, JUVENILE HORMONE ANALOGS, AND 6-OXOOCTANOIC ACID ON THE DEVELOPMENT OF THE MOSQUITO, CULEX TARSALIS (DIPTERA: CULICIDAE)

1974 ◽  
Vol 106 (1) ◽  
pp. 79-85 ◽  
Author(s):  
P. I. Ittycheriah ◽  
M. S. Quraishi ◽  
E. P. Marks
Keyword(s):  
Juvenile Hormone ◽  
Topical Treatment ◽  
Adult Emergence ◽  
Fourth Instar ◽  
Culex Tarsalis ◽  
Juvenile Hormone Analog ◽  
Hormone Analog ◽  
High Doses ◽  
Hormone Analogs ◽  
Very High

AbstractEggs, larvae, and pupae of Culex tarsalis Coquillett were treated with ecdysones, juvenile hormone analogs, and 6-oxooctanoic acid. Effects of these agents on mortality, induction of supernumerary stages, and adult emergence were determined. Topical treatment of eggs with CRD9499 (a juvenile hormone analog), β-ecdysone, and 22-isoecdysone caused a reduction in adult emergence. Treatment of fourth-instar larvae with these chemicals not only induced mortality but also caused the formation of supernumerary intermediate stages. Larvae of C. tarsalis were very susceptible to CRD9499, but pupae were resistant. The ecdysones caused some mortality but only at very high doses and would thus be of little use as larvicides. 6-Oxooctanoic acid caused high rates of mortality at 0.001 M concentrations.

scholarly journals Regulation of metamorphosis in neopteran insects is conserved in the paleopteran Cloeon dipterum (Ephemeroptera)

2021 ◽  
Vol 118 (34) ◽  
pp. e2105272118 ◽  
Author(s):  
Orathai Kamsoi ◽  
Alba Ventos-Alfonso ◽  
Fernando Casares ◽  
Isabel Almudi ◽  
Xavier Belles
Keyword(s):  
Juvenile Hormone ◽  
Molecular Analysis ◽  
Nymphal Instar ◽  
Morphological Studies ◽  
Flying Insects ◽  
Juvenile Hormone Analog ◽  
Hormone Analog ◽  
Two Stages ◽  
Cloeon Dipterum ◽  
Hormonal Treatments

In the Paleozoic era, more than 400 Ma, a number of insect groups continued molting after forming functional wings. Today, however, flying insects stop molting after metamorphosis when they become fully winged. The only exception is the mayflies (Paleoptera, Ephemeroptera), which molt in the subimago, a flying stage between the nymph and the adult. However, the identity and homology of the subimago still is underexplored. Debate remains regarding whether this stage represents a modified nymph, an adult, or a pupa like that of butterflies. Another relevant question is why mayflies have the subimago stage despite the risk of molting fragile membranous wings. These questions have intrigued numerous authors, but nonetheless, clear answers have not yet been found. By combining morphological studies, hormonal treatments, and molecular analysis in the mayfly Cloeon dipterum, we found answers to these old questions. We observed that treatment with a juvenile hormone analog in the last nymphal instar stimulated the expression of the Kr-h1 gene and reduced that of E93, which suppress and trigger metamorphosis, respectively. The regulation of metamorphosis thus follows the MEKRE93 pathway, as in neopteran insects. Moreover, the treatment prevented the formation of the subimago. These findings suggest that the subimago must be considered an instar of the adult mayfly. We also observed that the forelegs dramatically grow between the last nymphal instar, the subimago, and the adult. This necessary growth spread over the last two stages could explain, at least in part, the adaptive sense of the subimago.

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