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Heregulin enhances regenerative proliferation in postnatal rat utricular sensory epithelium after ototoxic damage

JOURNAL OF NEUROCYTOLOGY 1999年第10-11期28卷 901-912页

作者： Zheng, JL Frantz, G Lewis, AK Sliwkowski, M Gao, WQ Genentech Inc Dept Neurosci San Francisco CA 94080 USA Genentech Inc Dept Pathol San Francisco CA 94080 USA Genentech Inc Dept Mol Oncol San Francisco CA 94080 USA

Hair cell loss due to acoustic and ototoxic damage often leads to hearing and balance impairments. Although a spontaneous event in chicks and lower vertebrates, hair cell replacement occurs at a much lower frequency in mammals presumably due to a very low rate of supporting cell proliferation following injury. We report here that heregulin, a member of the neuregulin family, dramatically enhances proliferation of supporting cells in postnatal rat utricular epithelial sheet cultures after gentamicin treatment, as revealed by bromo-deoxyuridine (BrdU) immunocytochemistry. A dose-dependent study shows that the maximal effects of heregulin are achieved at 3 nM. The mitogenic effects of heregulin are confirmed in utricular whole mount cultures. Autoradiography of the utricular whole mount cultures shows that heregulin also enhances the number of tritiated thymidine-labeled cells within the hair cell layer. TaqMan quantitative RT-PCR analysis and immunocytochemistry reveal that heregulin and its binding receptors (ErbB-2, ErbB-3 and ErbB-4) are expressed in the inner ear sensory epithelium. Of several ligands activating various ErbB receptors, including heregulin, neuregulin-3, beta-cellulin, heparin binding-epidermal growth factor (HB-EGF), transforming growth factor-alpha (TGF-alpha) and EGF, heregulin shows the most potent mitogenic effects on supporting cells. Because neuregulin-3 that signals only through ErbB-4 does not show an effect, these data suggest that activation of the ErbB-2-ErbB-3 heterodimeric complexes, rather than ErbB-4, is critical for the proliferative response in the utricular sensory epithelium. In addition, gentamicin treatment induces an upregulation of heregulin mRNA. Considered together, heregulin may play an important role in hair cell regeneration following ototoxic damage.

关键词：细胞计数/药物作用细胞分裂/药物作用细胞培养的剂量效应关系药物内耳/代谢上皮细胞/细胞学上皮细胞/药物作用上皮细胞/代谢基因表达/药物作用庆大霉素类/药理学毛细胞听觉/细胞学毛细胞听觉/药物作用迷路支持细胞/细胞学迷路支持细胞/药物作用配体有丝分裂原/代谢有丝分裂原/毒性神经调节蛋白1/遗传学神经调节蛋白1/代谢神经调节蛋白1/药理学 RNA 信使/生物合成大鼠 Wistar 受体表皮生长因子/遗传学受体表皮生长因子/代谢受体 erbB-2/遗传学受体 erbB-2/代谢受体 erbB-3/遗传学受体 erbB-3/代谢再生/药物作用再生/生理学球囊和椭圆囊/细胞学球囊和椭圆囊/药物作用球囊和椭圆囊/代谢胸苷/代谢增量调节/药物作用动物大鼠

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Cellular communication in clone 9 cells exposed to magnetic fields

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RADIATION RESEARCH 2000年第5期153卷 690-698页

作者： Griffin, GD Williams, MW Gailey, PC Oak Ridge Natl Lab Div Life Sci Oak Ridge TN 37831 USA Ohio Univ Dept Phys & Astron Athens OH 45701 USA Oak Ridge Natl Lab Div Energy Oak Ridge TN 37831 USA

Magnetic-field exposure (45 Hz B-a.c. over a Bur density range of 7.7 to 49.9 mu T r.m.s. with parallel B-d.c. of 36.6 mu T) has been reported by Blackman and coworkers to inhibit gap junction intercellular communication in Clone 9 cells treated with chloral hydrate for 24 h prior to field exposure in accord with predictions of the ion parametric resonance model. The study reported here is an attempt to reproduce this effect. Baseline experiments showed that growth in culture and state of confluence at time of addition of chloral hydrate were comparable in both laboratories, PMA inhibited cell-cell communication in a dose-dependent manner, similar to the results of Blackman and coworkers, whereas cells in the present study were somewhat more sensitive to chloral hydrate than reported by Blackman and coworkers. A total of 38 exposure experiments were undertaken using a 45 Hz magnetic field with a Bur density of 23.8 mu T r.m.s., in parallel with a 36.6-mu T static magnetic field for 40 to 45 min, after pretreatment with 25 mM chloral hydrate for 24 h, In 14 unblinded experiments, a small but statistically significant effect of magnetic-field exposure was observed, but due to the subjective nature of the assay, it was deemed essential to carry out blinded experiments, The remaining 24 experiments were blinded. In 15 blinded experiments, cells purchased from the American Type Culture Collection and grown only in this laboratory were used, while in 9 experiments, the cells had originally been grown in Blackman's laboratory and were subsequently sent to this laboratory. There was no statistically significant effect of magnetic-field exposure on gap junction intercellular communication in these blinded experiments using either cell line. (C) 2000 Radiation Research Society.

关键词：致癌物/药理学细胞间通讯/药物作用细胞间通讯/辐射效应细胞计数/药物作用细胞计数/辐射效应细胞系水合氯醛/药理学克隆细胞/细胞学克隆细胞/辐射效应剂量效应关系药物剂量效应关系辐射电磁场/副作用缝隙接合部/药物作用缝隙接合部/辐射效应催眠药和镇静药/药理学肝/细胞学肝/辐射效应磁力学结果可重复性敏感性与特异性统计学非参数十四酰佛波乙酯/药理学动物大鼠

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Angiotensin II and basic fibroblast growth factor mitogenic pathways in human fetal mesangial cells

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PEDIATRIC RESEARCH 2000年第5期47卷 614-621页

作者： Izevbigie, EB Gutkind, JS Ray, PE Childrens Res Inst Childrens Natl Med Ctr Ctr Mol Physiol Res Washington DC 20010 USA NIDR Oral & Pharyngeal Canc Brach Program NIH Bethesda MD 20892 USA

Angiotensin II (Ang II) and basic fibroblast growth factor (bFGF/FGF-2) play relevant roles in renal development. Since the signaling pathways modulating the mitogenic effects of Ang LI and bFGF in human fetal mesangial cells (HFMc) are not clearly defined, we carried out experiments to determine whether they would exert their mitogenic effects by modulating the activity of the mitogen-activated protein kinases (MAPK) [extracellular signal-regulated kinase-2 (ERK-2)] and cAMP signaling pathways. In confluent HFMc, bFGF (20 ng/mL) induced a significant 4-fold increase in ERK-2 activity and [H-3]-thymidine incorporation (6-fold). In contrast, under similar tissue culture conditions, Ang II (10(-6) M) induced a more modest increase in ERK-2 activity (2-fold) and [H-3]-thymidine incorporation (35 +/- 4%). The mitogen-activated protein kinase kinase-l (MEK-1) inhibitor PD098059 (25 mu M) almost completely abolished the bFGF-induced proliferation in HFMc but did not significantly affect Ang II proliferative effects, In the presence of the cAMP elevating agent isoproterenol, Ang II and bFGF induced opposite changes in cAMP accumulation and cell growth. Isoproterenol inhibited the basal and bFGF-induced proliferation of HFMc through a MEK-1/2-independent pathway that included the accumulation of cAMP, In contrast, isoproterenol increased Ang II mitogenic effects in correlation with a reduction in cAMP accumulation. We conclude that Ang II and bFGF modulate the proliferation of HFMc through the stimulation of different MEK-1/2-dependent and independent signaling pathways. Activation of MEK-1/2 is required but not sufficient fur mitogenesis in HFMc. The accumulation of cAMP in HFMc counteracts the mitogenic effects of bFGF by a MEK-1/1-independent pathway.

关键词：肾上腺素能β激动剂/药理学血管紧张素Ⅱ/代谢血管紧张素Ⅱ/药理学细胞计数/药物作用细胞分裂/药物作用细胞培养的环AMP/代谢药物协同作用酶激活/药物作用酶抑制剂/药理学成纤维细胞生长因子2/代谢成纤维细胞生长因子2/药理学肾小球系膜/细胞学肾小球系膜/药物作用肾小球系膜/胚胎学肾小球系膜/代谢异丙肾上腺素/药理学 MAP激酶激酶1 MAP激酶激酶2 丝裂原活化蛋白激酶1/代谢丝裂原激活蛋白激酶激酶类/代谢丝裂原激活蛋白激酶类/代谢蛋白质丝氨酸苏氨酸激酶/代谢蛋白酪氨酸激酶类/代谢信号传导/药物作用胸苷/代谢人类

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Permeability, cytotoxicity, and genotoxicity of Cr(III) complexes and some Cr(V) analogues in V79 Chinese hamster lung cells

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CHEMICAL RESEARCH IN TOXICOLOGY 2000年第8期13卷 742-748页

作者： Dillon, CT Lay, PA Bonin, AM Cholewa, M Legge, GJF Univ Sydney Ctr Heavy Met Res Sch Chem Sydney NSW 2006 Australia Natl Occupat Hlth & Safety Commiss Sydney NSW 2001 Australia Univ Melbourne Sch Phys Micro Analyt Res Ctr Parkville Vic 3052 Australia Inst Phys Nucl Krakow Poland

The permeabilities and genotoxicities of the Cr(III) complexes [Cr(en)(3)](3+), mer-[Cr(glygly)(2)](-), cis-[Cr(phen)(2)(OH2)(2)](3+), and trans-[Cr(salen)(OH2)(2)](+) and the Cr(V) analogues of cis-[Cr(phen)(2)(OH2)(2)](3+) and trans-[Cr(salen)(OH2)(2)](+) [en being 1,2-ethanediamine, glygly being glycylglycine, phen being 1,10-phenanthroline, and salen being N,N'-ethylenebis(salicylideneiminato)] have been studied in V79 Chinese hamster lung cells. Following exposure of similar to 10(6) cells to 0.4 mM Cr(III) for 4 h, the Cr uptake by single cells was less than 10(-14) g/cell las determined by GFAAS analysis and as confirmed by PIXE analysis where the Cr concentration was below the limit of detection). Importantly, the Cr(V) analogue of cis-[Cr(phen)(2)(OH2)(2)] was significantly more permeable than the Cr(III) complex. The cytotoxicity of the Cr(III) complexes increased in the following order: mer-[Cr(glygly)(2)](-) < [Cr(en)(3)](3+) similar to cis-[Cr(phen)(2)(OH2)(2)](3+) < trans-[Cr(salen)(OH2)(2)](+). No genotoxic effects were observed following exposure to mer-[Cr(glygly)(2)](-) or [Cr(en)(3)](3+) at concentrations up to 6 mM. The Cr(III) imine complexes trans-[Cr(salen)(OH2)(2)](+) and cis-[Cr(phen)(2)(OH2)(2)](3+), which could be oxidized to Cr(V) complexes, induced MN in vitro at rates of 13.6 and 3.3 MN/1000 BN cells/mu mol of Cr, respectively. The comparative permeabilities and genotoxicities of trans-[Cr(salen)(OH2)(2)](+) and [CrO(salen)](+) were similar due to the instability of the Cr(V) complex at physiological pH values (7.4). There was a substantial increase in the permeability of [Cr(O)(2)(phen)(2)](+), compared to that of the Cr(III) analogue, which was accompanied by a highly genotoxic response. Consequently, any Cr(III) complex that is absorbed by cells and can be oxidized to Cr(V) must be considered as a potential carcinogen. This has potential implications for the increased use of Cr(III) complexes as dietary supplements and highlights the

关键词：细胞计数/药物作用细胞系细胞膜通透性细胞存活/药物作用铬化合物/药代动力学铬化合物/毒性仓鼠亚科仓鼠属剂量效应关系药物电子探针微区分析肺/细胞学肺/药物作用肺/代谢微核试验诱变剂/药代动力学诱变剂/毒性动物

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Nicotine regulates basic fibroblastic growth factor and transforming growth factorβ₁ production in endothelial cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第2期257卷 306-312页

作者： Cucina, A Corvino, V Sapienza, P Borrelli, V Lucarelli, M Scarpa, S Strom, R Santoro-D'Angelo, L Cavallaro, A Univ Rome La Sapienza Dept Surg 1 Rome Italy Univ Rome La Sapienza Dept Cellular Biotechnol & Hematol Rome Italy Univ Rome La Sapienza Dept Med Histol & Embryol Rome Italy

Nicotine, a constituent of cigarette smoking, may induce atherosclerosis through the production of growth factors. The pattern of bFGF and TGF beta(1) production and release by bovine aortic endothelial cells (EC) stimulated with nicotine (from 6 x 10(-4) to 6 x 10(-8) M) was studied. EC viability and count were assessed. The presence of bFGF and TGF beta(1) in serum-free conditioned media was determined by the inhibition antibody-binding assay and Western blot analysis. Mitogenic activity of nicotine on EC was also determined. Polymerase chain reaction (PCR) was used to study the expression of bFGF and TGF beta(1). The bFGF release after nicotine stimulation was greater than controls, whereas TGF beta(1) release was lower. At a nicotine concentration of 6 x 10(-6) M we noted the greatest mitogenic activity. The addition of monoclonal antibody anti-bFGF decreased the tritiated thymidine uptake of EC exposed to nicotine but the addition of monoclonal antibody anti-TGF beta(1) had no significant effect, bFGF mRNA expression was significantly higher in EC exposed to nicotine than in controls, whereas TGF beta(1) mRNA expression was not modified. From these data we concluded that nicotine regulates bFGF production and release and TGF beta(1) release and may have a key role in the development and progression of atherosclerosis. (C) 1999 Academic Press.

关键词：抗体单克隆/药理学主动脉动脉硬化/病因学动脉硬化/代谢印迹法蛋白质细胞计数/药物作用细胞分裂/药物作用细胞存活/药物作用培养基条件性/药理学 DNA/生物合成剂量效应关系药物内皮血管/细胞学内皮血管/药物作用内皮血管/代谢内皮血管/病理学成纤维细胞生长因子2/遗传学成纤维细胞生长因子2/免疫学成纤维细胞生长因子2/代谢有丝分裂原/代谢有丝分裂原/药理学肌平滑/细胞学肌平滑/药物作用尼古丁/药理学尼古丁/毒性聚合酶链反应 RNA 信使/代谢转化生长因子β/遗传学转化生长因子β/免疫学转化生长因子β/代谢动物牛

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Insulin like growth factor-1 receptors mediate infragenicular vascular smooth muscle cell proliferation in response to glucose and insulin not by insulin receptors

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AMERICAN JOURNAL OF SURGERY 1999年第2期178卷 156-161页

作者： Avena, R Mitchell, ME Carmody, B Arora, S Neville, RF Sidawy, AN George Washington Univ Vet Affairs Med Ctr Dept Surg Washington DC USA Georgetown Univ Med Ctr Washington DC 20007 USA

PURPOSE: Vascular smooth muscle cell (VSMC) proliferation is an early event in the pathogenesis of atherosclerosis. Insulin and glucose are known to stimulate the growth of VSMC, Cell membrane receptors play an important role in the proliferation of VSMC in response to growth factors. Insulin and insulin-like growth factor-1 (IGF-1) have demonstrated a cross reactivity for receptor binding and function. By using monoclonal antibodies directed against insulin (IRA) and IGF-1 (IGF-IRA) receptors, we attempt to further delineate the mechanism for the proliferation of VSMC in response to insulin and glucose. METHODS: Human infragenicular VSMC isolated from diabetic patients undergoing below-knee amputations were used. Cells from passages 3 to 6 were grown in serum-free media with a glucose concentrations of 0.1% or 0.2%, both with and without insulin (100 ng/mL). The baseline cell density was 4,635 +/- 329 cells/mL, IRA or IGF-1RA was added to the media, with the control group receiving neither antibody. Cells were grown in 5% CO2 at 37 degrees C for 6 days. Analysis of variance was used for statistical analysis, with P <0.05 considered significant. In addition, DNA synthesis was measured using thymidine incorporation assays in the same groups of cells receiving IRA, IGF-IRA, and no antibody. RESULTS: IGF-1RA prevented the proliferation of VSMC in response to insulin and glucose, while IRA had no effect on cell growth. There was no significant growth when IGF-1RA was added to the media, while the control group and the group receiving IRA demonstrated significant growth compared with the baseline concentration of 4,635 +/- 329 cells/mL at all concentrations of insulin and glucose. [H-3]thymidine incorporation assays confirmed the cell count results. CONCLUSIONS: These results suggest that the mitogenic effects of insulin and glucose on infragenicular VSMC are due to stimulation of the IGF-I receptor. VSMC antiproliferative strategies employing receptor blockade should be

关键词：方差分析抗体单克隆/诊断应用动脉硬化/病因学动脉硬化/病理学细胞计数/药物作用细胞分裂/药物作用细胞分裂/生理学细胞培养的交叉反应培养基无血清 DNA/生物合成糖尿病/病理学葡萄糖/投药和剂量葡萄糖/药理学胰岛素/投药和剂量胰岛素/药理学有丝分裂原/投药和剂量有丝分裂原/药理学肌平滑血管/细胞学肌平滑血管/药物作用放射性药物/诊断应用受体 IGF1型/药物作用受体 IGF1型/生理学受体胰岛素/药物作用受体胰岛素/生理学胸苷/代谢氚/诊断应用人类

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Down-regulation of nucleophosmin/B23 mRNA delays the entry of cells into mitosis

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第3期257卷 865-870页

作者： Jiang, PS Yung, BYM Chang Gung Univ Coll Med Dept Pharmacol Canc Biochem Lab Tao Yuan 333 Taiwan

In investigating the regulation of nucleophosmin/B23 mRNA expression at the entry of mitosis, the results of Northern gel blot analysis showed that the nucleophosmin/B23 mRNA levels significantly increased in prometaphase (nocodazole-arrested) or metaphase (colchicine-arrested) cells collected by mitotic shake-off. A higher level of nucleophosmin/B23 mRNA was detected in all the collected mitotic cells arrested by treatment with nocodazole for 10-18h as compared to that in G(2) cells. An attempt was then made to determine whether the regulation of nucleophosmin/B23 mRNA plays a role in the control of entry into mitosis. Down-regulation of nucleophosmin/B23 mRNA by transfection of its antisense construct resulted in the delay of cells entering mitosis. The demonstration of the characteristic changes in the mRNA level of nucleophosmin/B23 during the entry of cells into mitosis implicates the importance of nucleophosmin/B23 in the control of the mitotic fate of nucleoli and cell growth, (C) 1999 Academic Press.

关键词：反义成分(遗传学)/遗传学细胞黏附/药物作用细胞计数/药物作用细胞存活/药物作用秋水仙碱/药理学减量调节 HeLa细胞分裂间期/药物作用中期/药物作用有丝分裂/药物作用有丝分裂指数/药物作用诺考达唑/药理学核蛋白质类/遗传学 RNA 信使/代谢胸苷/药理学时间因素转染人类

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Insulin-mediated cell proliferation and survival involve inhibition of c-Jun N-terminal kinases through a phosphatidylinositol 3-kinase- and mitogen-activated protein kinase phosphatase-1-dependent pathway

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ENDOCRINOLOGY 2000年第3期141卷 922-931页

作者： Desbois-Mouthon, C Cadoret, A Blivet-Van Eggelpoël, MJ Bertrand, F Caron, M Atfi, A Cherqui, G Capeau, J Univ Paris 06 INSERM U402 F-75571 Paris 12 France Hop St Antoine INSERM U482 F-75571 Paris 12 France

We previously reported that long term treatment with insulin led to sustained inhibition of c-Jun N-terminal kinases (JNKs) in CHO cells overexpressing insulin receptors. Here we investigated the sig -naling molecules involved in insulin inhibition of JNKs, focusing on phosphatidylinositol 3-kinase (PI 3-K) and mitogen-activated protein kinase phosphatase-1 (MKP-1). In addition, we examined the relevance of JNK inhibition for insulin-mediated proliferation and survival. Insulin inhibition of JNKs was mediated by PI 3-K, as it was blocked by wortmannin and LY294002 and required the de novo synthesis of a phosphatase(s), as it was abolished by orthovanadate and actinomycin D. MKP-1 was a good candidate because 1) insulin stimulation of MKP-1 expression correlated with insulin inhibition of JNKs: 2) insulin stimulation of MKP-1 expression, like insulin inhibition of JNKs, was mediated by PI 3-K;and 3) the transient expression of an antisense MKP-1 RNA reduced the insulin inhibitory effect on JNKs. The overexpression of a dominant negative JNK1 mutant increased insulin stimulation of DNA synthesis and mimicked the protective effect of insulin against serum withdrawal-induced apoptosis. The overexpression of wild-type JNK1 or antisense MKP-1 RNA reduced the proliferative and/or antiapoptotic responses to insulin. Altogether, these results demonstrate that insulin inhibits JNKs through a PI 3-K and MW-1-dependent pathway and provide evidence for a key role for JNK inhibition in insulin regulation of proliferation and survival.

关键词： 1-磷脂酰肌醇3-激酶/遗传学 1-磷脂酰肌醇3-激酶/代谢细胞凋亡/药物作用印迹法蛋白质 CHO细胞细胞计数/药物作用细胞周期蛋白质类细胞分裂/生理学细胞存活/生理学细胞培养的仓鼠亚科 DNA/生物合成 DNA/遗传学糖原/生物合成即早蛋白质类/遗传学即早蛋白质类/代谢胰岛素/生理学 JNK丝裂原活化蛋白激酶类丝裂原激活蛋白激酶类/拮抗剂和抑制剂丝裂原激活蛋白激酶类/遗传学质粒/遗传学信号传导/遗传学信号传导/生理学转染/遗传学动物大鼠

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Expression of functional tyrosine kinases on immortalized Kaposi's sarcoma cells

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JOURNAL OF CELLULAR PHYSIOLOGY 2000年第2期184卷 246-254页

作者： Montaldo, F Maffé, A Morini, M Noonan, D Giordano, S Albini, A Prat, M Univ Piemonte Orientale Dept Med Sci Sch Med I-28100 Novara Italy Univ Turin Sch Med Inst Canc Res Div Mol Oncol Turin Italy Ist Nazl Ric Canc Ctr Biotecnol Avanzate I-16132 Genoa Italy

Kaposi's sarcoma (KS) is the most frequent malignant lesion in patients with AIDS and is characterized by spindle cell proliferation, inflammatory cell infiltration, angiogenesis, edema, and invasiveness. KS origin is still debated. The complex aspect of this disease is probably supported by multiple concomitant pathogenetic factors, among which growth factors and their cognate tyrosine kinase receptors are deeply involved. Here we have investigated the expression status and functional integrity of KDR and Met receptors, as well as of their ligands, in an immortalized KS cell line (KS-IMM). The MET and KDR genes encode the tyrosine kinase receptors for Hepatocyte Growth Factor (HGF) and Vascular Endothelial Growth Factor (VEGF) respectively. Both factors are pleiotropic cytokines controlling growth, survival, motility, invasive migration and differentiation of endothelial cells. We have found that KS-IMM cells, which retain most of the features of the parental tumor and can induce KS-like sarcomas when injected subcutaneously in nude mice, express the Met receptor, but not its ligand. The receptor, which is basally inactive, is functional, being tyrosine phosphorylated in response to ligand stimulation and mediating the expected HGF-dependent biological responses of motility, invasion and proliferation. Moreover, we report that KS-IMM cells coexpress VEGF and KDR and that KDR is constitutively tyrosine phosphorylated, possibly as a consequence of the establishment of an autocrine loop. The receptor, however, maintains responsiveness to exogenously added ligand, by increasing the level of tyrosine phosphorylation and by responding in biological assays of motility, invasion and proliferation. Finally, we have found that the two growth factors synergize in a motility assay. These data show that HGF and VEGF are growth factors active on KS-IMM cells. J. Cell. Physiol. 184:246-254, 2000. (C) 2000 Wiley-Liss, Inc.

关键词：细胞计数/药物作用内皮生长因子/药理学肝细胞生长因子/药理学淋巴因子/药理学蛋白质亚型/药理学蛋白酪氨酸激酶类/生物合成蛋白酪氨酸激酶类/药物作用肉瘤卡波西/酶学肿瘤细胞培养的血管内皮生长因子A 血管内皮生长因子类动物人类小鼠

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Sublethal lead affects pituitary function of rainbow trout during exogenous vitellogenesis

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ARCHIVES OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY 2000年第1期38卷 46-51页

作者： Ruby, SM Hull, R Anderson, P Concordia Univ Dept Biol Ecotoxicol Lab Montreal PQ H3G 1M8 Canada

Sexually maturing female rainbow trout, Oncorhynchus mykiss, were exposed to 10 mu g/L of waterborne lead Pb(NO3)(2) for 12 days during endogenous vitellogenesis and 12 days during exogenous vitellogenesis. Lead had no significant effect on either gonadosomatic indices or mean maximum diameters of developing oocytes during early vitellogenesis. When females were exposed during exogenous vitellogenesis, however, both GSI and oocyte growth were significantly different from controls on day 12. Similarly GSI and oocyte growth was significantly reduced in lead-exposed fish. Atomic absorption spectroscopy measurements of lead levels in liver, ovaries, and blood tissues showed significant levels of lead in the blood. Lead did not accumulate in either the ovaries or the liver. Analysis of pituitary basophils during both endogenous and exogenous vitellogenesis and subsequent comparison with reproductive parameters in the ovaries indicated that GtH-basophils did not significantly increase in controls during endogenous vitellogenesis, and there was no significant change in GSI or ovarian growth in either controls or lead-exposed females. However during exogenous vitellogenesis, control basophils significantly increased over the 12-day experiment, but were not significantly different over 12 days in lead-exposed females. Both GSI and oocyte growth were significantly different from controls in lead-exposed females. The results suggest that naturally occurring changes in GTH-producing basophils during vitellogenesis alters GSI and oocyte growth in female rainbow trout exposed to lead during exogenous vitellogenesis, but not during endogenous vitellogenesis.

关键词：细胞计数/药物作用铅/血液铅/毒性硝酸盐类/血液硝酸盐类/毒性大麻哈鱼裂喉/生理学卵母细胞/药物作用卵母细胞/病理学器官测量/药物作用卵巢/化学卵巢/药物作用卵巢/病理学垂体/药物作用垂体/代谢垂体/病理学卵黄发生/药物作用水污染物化学性/血液水污染物化学性/毒性动物女(雌)性

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