title: Insight into the mechanism of reproductive dysfunction caused by neonicotinoid pesticides.
abstract: Neonicotinoids, which were developed in the 1990 s as an insecticide having selective toxicity, were later found to cause reproductive abnormalities in experimental animals. In Japan there is an attempt to preserve endangered animals, including the Japanese crested ibis, and there is a question of whether neonicotinoids affect the reproduction of this bird, since they are used in its habitat. Hence, we investigated whether the daily oral administration of the neonicotinoid clothianidin (CTD) has any deleterious effects on the reproductive function of mature male only or both young male and female quails as experimental animals. Vacuolization and the number of germ cells having fragmented DNA in seminiferous tubules, as well as the number and size of vacuoles in hepatocytes, increased dose-dependently. The ovaries showed abnormal histology in the granulosa cells, which produce progesterone. There were significant differences in egg-laying rates and embryo weights between the groups. Glutathione Peroxidase 4 (GPx4) and Manganese Superoxide Dismutase (Mn-SOD), which protect the organism from oxidative damage, showed a dose-dependent decrease. Thus, it is possible neonicotinoids affect the bird's reproductive system through oxidative stress, reflecting an imbalance between the production of reactive oxygen species (ROS) and a biological system's ability to readily detoxify the reactive intermediates or easily repair the resulting damage. Responding to our study, Sado Island has since succeeded in breeding Japanese crested ibis in the wild without the use of neonicotinoids.
authors.affiliation: Laboratory of Molecular Morphology, Department of Animal Science, Graduate School of Agricultural Science, Kobe University.
authors.forename: Nobuhiko
authors.initials: N
authors.lastname: Hoshi
authors.forename: Tetsushi
authors.initials: T
authors.lastname: Hirano
authors.forename: Takuya
authors.initials: T
authors.lastname: Omotehara
authors.forename: Junko
authors.initials: J
authors.lastname: Tokumoto
authors.forename: Yuria
authors.initials: Y
authors.lastname: Umemura
authors.forename: Youhei
authors.initials: Y
authors.lastname: Mantani
authors.forename: Takashi
authors.initials: T
authors.lastname: Tanida
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Warita
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Tabuchi
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Yokoyama
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kitagawa
mesh_terms: D000818:Animals; D053938:DNA Fragmentation; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D006146:Guanidines / Q000633:toxicity*; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007306:Insecticides / Q000633:toxicity*; D008297:Male; D000073943:Neonicotinoids; D010053:Ovary / Q000187:drug effects / Q000473:pathology; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D011784:Quail / Q000502:physiology*; D012098:Reproduction / Q000187:drug effects*; D012671:Seminiferous Tubules / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism; D013844:Thiazoles / Q000633:toxicity*
chemical_list: D006146:Guanidines; D007306:Insecticides; D000073943:Neonicotinoids; D013844:Thiazoles; C480342:clothianidin; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase