PubMed:23851285 JSONTXT

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Results showed that PTTH treatment resulted in a rapidly transient increase in the intracellular ROS concentration, as measured using 2',7'-dichlorofluorescin diacetate (DCFDA), an oxidation-sensitive fluorescent probe. The antioxidant, N-acetylcysteine (NAC), abolished PTTH-induced increase in fluorescence. Furthermore, PTTH-induced ROS production was partially inhibited by the NAD(P)H oxidase inhibitor, apocynin, indicating that NAD(P)H oxidase is one of the sources for PTTH-stimulated ROS production. Four mitochondrial oxidative phosphorylation inhibitors (rotenone, antimycin A, the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), and diphenylene iodonium (DPI)) significantly attenuated ROS production induced by PTTH. These data suggest that the activity of complexes I and III in the electron transport chain and the mitochondrial inner membrane potential (ΔΨ) contribute to PTTH-stimulated ROS production. In addition, PTTH-stimulated ecdysteroidogenesis was greatly inhibited by treatment with either NAC or mitochondrial inhibitors (rotenone, antimycin A, FCCP, and DPI), but not with apocynin. These results indicate that mitochondria-derived, but not membrane NAD(P)H oxidase-mediated ROS signaling, is involved in PTTH-stimulated ecdysteroidogenesis of PGs in B. mori."}

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Results showed that PTTH treatment resulted in a rapidly transient increase in the intracellular ROS concentration, as measured using 2',7'-dichlorofluorescin diacetate (DCFDA), an oxidation-sensitive fluorescent probe. The antioxidant, N-acetylcysteine (NAC), abolished PTTH-induced increase in fluorescence. Furthermore, PTTH-induced ROS production was partially inhibited by the NAD(P)H oxidase inhibitor, apocynin, indicating that NAD(P)H oxidase is one of the sources for PTTH-stimulated ROS production. Four mitochondrial oxidative phosphorylation inhibitors (rotenone, antimycin A, the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), and diphenylene iodonium (DPI)) significantly attenuated ROS production induced by PTTH. These data suggest that the activity of complexes I and III in the electron transport chain and the mitochondrial inner membrane potential (ΔΨ) contribute to PTTH-stimulated ROS production. In addition, PTTH-stimulated ecdysteroidogenesis was greatly inhibited by treatment with either NAC or mitochondrial inhibitors (rotenone, antimycin A, FCCP, and DPI), but not with apocynin. These results indicate that mitochondria-derived, but not membrane NAD(P)H oxidase-mediated ROS signaling, is involved in PTTH-stimulated ecdysteroidogenesis of PGs in B. mori."}

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{"project":"Allie","denotations":[{"id":"SS1_23851285_1_0","span":{"begin":180,"end":203},"obj":"expanded"},{"id":"SS2_23851285_1_0","span":{"begin":205,"end":208},"obj":"abbr"},{"id":"SS1_23851285_1_1","span":{"begin":213,"end":239},"obj":"expanded"},{"id":"SS2_23851285_1_1","span":{"begin":241,"end":245},"obj":"abbr"},{"id":"SS1_23851285_1_2","span":{"begin":293,"end":311},"obj":"expanded"},{"id":"SS2_23851285_1_2","span":{"begin":313,"end":316},"obj":"abbr"},{"id":"SS1_23851285_2_0","span":{"begin":470,"end":504},"obj":"expanded"},{"id":"SS2_23851285_2_0","span":{"begin":506,"end":511},"obj":"abbr"},{"id":"SS1_23851285_3_0","span":{"begin":573,"end":589},"obj":"expanded"},{"id":"SS2_23851285_3_0","span":{"begin":591,"end":594},"obj":"abbr"},{"id":"SS1_23851285_5_0","span":{"begin":1002,"end":1022},"obj":"expanded"},{"id":"SS2_23851285_5_0","span":{"begin":1024,"end":1027},"obj":"abbr"}],"relations":[{"id":"AE1_23851285_1_0","pred":"abbreviatedTo","subj":"SS1_23851285_1_0","obj":"SS2_23851285_1_0"},{"id":"AE1_23851285_1_1","pred":"abbreviatedTo","subj":"SS1_23851285_1_1","obj":"SS2_23851285_1_1"},{"id":"AE1_23851285_1_2","pred":"abbreviatedTo","subj":"SS1_23851285_1_2","obj":"SS2_23851285_1_2"},{"id":"AE1_23851285_2_0","pred":"abbreviatedTo","subj":"SS1_23851285_2_0","obj":"SS2_23851285_2_0"},{"id":"AE1_23851285_3_0","pred":"abbreviatedTo","subj":"SS1_23851285_3_0","obj":"SS2_23851285_3_0"},{"id":"AE1_23851285_5_0","pred":"abbreviatedTo","subj":"SS1_23851285_5_0","obj":"SS2_23851285_5_0"}],"text":"Involvement of reactive oxygen species in PTTH-stimulated ecdysteroidogenesis in prothoracic glands of the silkworm, Bombyx mori.\nIn the present study, the possible involvement of reactive oxygen species (ROS) in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis of Bombyx mori prothoracic glands (PGs) was investigated. Results showed that PTTH treatment resulted in a rapidly transient increase in the intracellular ROS concentration, as measured using 2',7'-dichlorofluorescin diacetate (DCFDA), an oxidation-sensitive fluorescent probe. The antioxidant, N-acetylcysteine (NAC), abolished PTTH-induced increase in fluorescence. Furthermore, PTTH-induced ROS production was partially inhibited by the NAD(P)H oxidase inhibitor, apocynin, indicating that NAD(P)H oxidase is one of the sources for PTTH-stimulated ROS production. Four mitochondrial oxidative phosphorylation inhibitors (rotenone, antimycin A, the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), and diphenylene iodonium (DPI)) significantly attenuated ROS production induced by PTTH. These data suggest that the activity of complexes I and III in the electron transport chain and the mitochondrial inner membrane potential (ΔΨ) contribute to PTTH-stimulated ROS production. In addition, PTTH-stimulated ecdysteroidogenesis was greatly inhibited by treatment with either NAC or mitochondrial inhibitors (rotenone, antimycin A, FCCP, and DPI), but not with apocynin. These results indicate that mitochondria-derived, but not membrane NAD(P)H oxidase-mediated ROS signaling, is involved in PTTH-stimulated ecdysteroidogenesis of PGs in B. mori."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":850,"end":863},"obj":"HP_0001427"},{"id":"T2","span":{"begin":1187,"end":1200},"obj":"HP_0001427"},{"id":"T3","span":{"begin":1380,"end":1393},"obj":"HP_0001427"}],"text":"Involvement of reactive oxygen species in PTTH-stimulated ecdysteroidogenesis in prothoracic glands of the silkworm, Bombyx mori.\nIn the present study, the possible involvement of reactive oxygen species (ROS) in prothoracicotropic hormone (PTTH)-stimulated ecdysteroidogenesis of Bombyx mori prothoracic glands (PGs) was investigated. Results showed that PTTH treatment resulted in a rapidly transient increase in the intracellular ROS concentration, as measured using 2',7'-dichlorofluorescin diacetate (DCFDA), an oxidation-sensitive fluorescent probe. The antioxidant, N-acetylcysteine (NAC), abolished PTTH-induced increase in fluorescence. Furthermore, PTTH-induced ROS production was partially inhibited by the NAD(P)H oxidase inhibitor, apocynin, indicating that NAD(P)H oxidase is one of the sources for PTTH-stimulated ROS production. Four mitochondrial oxidative phosphorylation inhibitors (rotenone, antimycin A, the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), and diphenylene iodonium (DPI)) significantly attenuated ROS production induced by PTTH. These data suggest that the activity of complexes I and III in the electron transport chain and the mitochondrial inner membrane potential (ΔΨ) contribute to PTTH-stimulated ROS production. In addition, PTTH-stimulated ecdysteroidogenesis was greatly inhibited by treatment with either NAC or mitochondrial inhibitors (rotenone, antimycin A, FCCP, and DPI), but not with apocynin. These results indicate that mitochondria-derived, but not membrane NAD(P)H oxidase-mediated ROS signaling, is involved in PTTH-stimulated ecdysteroidogenesis of PGs in B. mori."}