Effects of fine particulate matter (PM2.5) on ovarian function and embryo quality in mice.

Fine particulate matter (PM2.5) has an adverse effect on reproductive function, in particular causing reduced male reproductive function, but relatively few studies have directly targeted its effects on female reproduction. To investigate the effects of PM2.5 exposure on female reproduction, we exposed female mice to PM2.5 by intratracheal instillation for 28 days, and evaluated apoptosis of ovarian granulosa cells and oocytes and the quality embryos after insemination. Our results showed increased numbers of apoptotic granulosa cells and oocytes after exposure to elevated concentrations of PM2.5, which had adverse effects on female fertility via compromising embryo development and quality. We conclude that PM2.5 induced apoptosis of ovarian granulosa cells and oocytes leading to disrupted embryo development and female fertility in mice.

Effects of Prenatal PM10 Exposure on Fetal Cardiovascular Malformations in Fuzhou, China: A Retrospective Case-Control Study.

BACKGROUND: Maternal exposure to ambient air pollution has been associated with an increased risk of congenital heart defects in offspring; however, the results are inconsistent. OBJECTIVES: We investigated whether there is an association between prenatal exposure to particulate matter with diameter ≤10µm (PM10) during early pregnancy and fetal cardiovascular malformations. METHODS: The gravidae from a hospital-based case­control study in Fuzhou, China, during 2007­2013 were assigned 10-d or 1-mo averages of daily PM10 using an air monitor­based inverse distance weighting method during early pregnancy. A total of 662 live-birth or selectively terminated cases and 3,972 live-birth controls were enrolled. The exposure was considered as a categorical variable. A multivariable logistic regression model was constructed to quantify the adjusted odds ratios (aORs) of the exposure to PM10 and the risks of fetal cardiovascular malformations. RESULTS: PM10 levels were positively associated with the risks of atrial septal defect (aORs ranging from 1.29 to 2.17), patent ductus arteriosus [aORs = 1.54, 1.63; 95% confidence intervals (CIs): 1.17, 2.23; 1.06, 3.24], overall fetal cardiovascular malformations (aOR = 1.28; 95% CI: 1.03, 1.61), ventricular septal defect (aOR = 1.19; 95% CI: 1.00, 1.43), and tetralogy of Fallot (aOR = 1.44; 95% CI: 1.01, 2.19) in the various observed periods scaled by 10 d or 1 mo in the first and second gestation months. The strongest associations were observed for exposure to PM10 in the second quartile, whereas the associations were attenuated when higher concentrations of PM10 in the third and fourth quartiles of the exposure were evaluated. No correlations of PM10 levels with these cardiovascular malformations in the other time periods of gestation were observed. CONCLUSIONS: Our findings suggest some positive associations between maternal exposure to ambient PM10 during the first two months of pregnancy and fetal cardiovascular malformations. https://doi.org/10.1289/EHP289.

[Effect of airborne particulate matter exposure on pregnancy and fetal development in female mice].

OBJECTIVE: To investigate subacute exposure of airborne particulate matter (PM) on pregnancy and fetal development in female mice. METHODS: Forty female and forty male ICR adult mice were caged separately by 1:1 to get access to pregnancy. The pregnant mice were randomized into control group (A), small (B), middle (C), large (D) or overdose (E) PM challenge groups (n = 8-11), and were administered with 30 µl of phosphate buffered solution (A) or resuspended standard PM SRM 1649a at 0.09 (B), 0.52 (C), 1.85 (D) or 69.2 (E) µg/µl, once per trid from d 0 till d 19 of pregnancy via instillation onto the base of the tongue. Fetal mice were harvested by cesarean section at the time when spontaneous delivery occurred. Body weight of the pregnant mice, gestational days, intrauterine survival and growth, hepatic and pneumonic histopathological changes of the fetal mice were investigated. Lung/body and liver/body weight ratios were calculated. Expressions of mRNA and protein of CYP1A1 in the fetal lung and CYP1A2 in the fetal liver were assayed. RESULTS: (1) All of the pregnant mice survived pregnancy throughout the entire experiment. Body weight of the pregnant mice was not significantly different among all the groups at gestational d 1 and 7 (P > 0.05), but significantly lower in group E [(41.8 ± 5.8) and (48.9 ± 8.9) g] than in group A [(45.9 ± 1.8) and (56.2 ± 4.9) g] at gestational d 14 and 18 (P < 0.05). The gestational days were significantly decreased in group E [(19.3 ± 1.3) d] when compared with group A [(20.5 ± 0.7) d; P < 0.05] and were not significantly different among groups A, B, C and D (P > 0.05). Lung/body and liver/body weight ratios of the fetal mice were significantly increased in group E [(1.21 ± 0.18) and (4.68 ± 0.21)%] as compared with groups A, B, C and D (P < 0.05). (2) Mortality rates of the fetuses were significantly higher in group E (23.0%) than in groups A (0.8%), B (0.9%), C (1.7%) and D (3.7%) (P < 0.05), but were not significantly different among groups A, B, C and D (P > 0.05) despite of an increasing tendency. (3) Pathological changes in the liver and lung of the fetuses were conspicuous in group E. The fetal liver injury was histopathologically evidenced by deranged tissue structure, degenerated parenchyma of hepatic cells, and mildly stained cytoplasm. Adipose degeneration was represented by clear-boundary intracytoplasmic vacuoles in most of the liver cells, and cell pyknosis with heavily stained cytoplasm was observed in some of the liver cells. Inflammatory cell infiltration and focal necrosis were occasionally found in the hepatic tissue. The fetal lung exhibited bronchiole with narrow lumina, vascular engorgement in the submucosal layer, interstitial and alveolar edema, thickened alveolar septum, granulocyte and lymphocyte infiltrations within the pulmonary alveoli and around the bronchioles. The above pathological changes were lesser in groups C and D, and were not or least found in groups A and B. (4) Protein expressions of CYP1A1 in the fetal lung and CYP1A2 in the fetal liver were significantly increased in group E (1.20 ± 0.40 and 2.55 ± 0.89) when compared with group A (0.77 ± 0.36 and 2.08 ± 0.31) (P < 0.05). mRNA expressions of CYP1A1 in the fetal lung were significantly increased in groups C (0.36 ± 0.12), D (0.41 ± 0.08) and E (0.43 ± 0.11) compared with group A (0.21 ± 0.10), and significantly increased in groups D and E compared with group B (0.28 ± 0.10, P < 0.05). mRNA expressions of CYP1A2 in the fetal liver were significantly increased in groups C (0.37 ± 0.13), D (0.36 ± 0.14) and E (0.43 ± 0.16) compared with group A (0.21 ± 0.03), and significantly increased in group E compared with group B (0.24 ± 0.11, P < 0.05). CONCLUSIONS: PM elicited embryotoxigenicity and resulted in adverse pregnancy outcomes in mice by intrauterine exposure of overdose PM. The expressions of cancer-related genes CYP1A1 and CYP1A2 were up-regulated in organs after the middle- and large-dose subacute exposure of PM, which may have a potential role on the future development.

[Instillation of diesel exhaust particles on the posterior wall of pharynx on reproductive function in female mice].

OBJECTIVE: The present work aims to investigate the effects of subacute exposure to diesel exhaust particles (DEP) on reproductive function in female mice. METHODS: A total of 168 ICR (Institute of Cancer Research) mice were randomly divided into four groups by numeration table method, including the low (B), middle (C), high (D) dose DEP exposure groups and the control group (A). Each group consisted of 42 mice. Mice were inoculated with 30 µl DEP suspension at 0.8 (B), 3.0 (C), 12.0 (D) µg/µl, respectively, or the same volume of phosphate-buffered saline (A) on pharynx posterior wall per triduum for 4 times. The body weight and ovary weight were tested and ovary weight/body weight ratios were calculated. Rates of survival, germinal vesicle breakdown, extrusion of the first polar body, in-vitro fertilization and quantity of mitochondrial DNA for the oocytes were investigated. Ultrastructural changes of the oocytes were observed. RESULTS: The ovary weight/body weight ratios were (15.4 ± 7.3) × 10(-5), (14.1 ± 6.8) × 10(-5), (8.2 ± 0.7) × 10(-5) and (7.2 ± 2.5) × 10(-5) in groups A, B, C and D (F = 3.841, P < 0.05). In groups A, B, C and D at 48 h post-insemination, rates of oocyte survival were 64.3%, 56.8%, 39.5% and 32.9% (χ(2) = 21.575, P < 0.05), rates of extrusion of the first polar body were 75.5%, 65.3%, 37.0% and 27.1% (χ(2) = 52.772, P < 0.05), rates of 2-cell embryos were 27.9%, 39.1%, 17.6% and 12.5% (χ(2) = 20.148, P < 0.05), and rates of embryos over 2 cells were 45.3%, 32.2%, 12.5% and 13.9% (χ(2) = 32.135, P < 0.05), respectively, and were significantly lower in groups C and D compared with group A (P < 0.05). Logarithmic values of mitochondrial DNA copy numbers were 6.54 ± 0.13, 6.48 ± 0.09, 5.57 ± 0.15 and 5.41 ± 0.07 in groups A, B, C and D, respectively, and were significantly lower in groups C and D compared with group A or B (F = 89.241, P < 0.05). A number of mitochondria of the oocytes exhibited tremendous tumescence and vacuolization in groups C and D, which was contrast to a roughly normal appearance in groups A and B. CONCLUSIONS: DEP is noxious to murine female reproduction. Subacute exposure to DEP injures the ovary and oocyte resulting in compromised ovarian function and fertilizability of the oocyte.

[Changes and significance of orphanin and serotonin in patients with postpartum depression].

OBJECTIVE: To study the changes of orphanin (OFQ) and serotonin (5-HT) in the patients with postpartum depression (PPD). METHODS: Twenty one patients with postpartum depression (PPD group) and 25 healthy lying-in women (control group) were studied. The concentrations of plasma OFQ were measured by radioimmunoassay. The levels of 5-HT were measured with high-pressure liquid chromatography with electrochemical detector. RESULTS: (1) The levels of plasma OFQ in PPD group were (28.5 +/- 5.8) ng/L, in control group, the levels of OFQ was (10.4 +/- 3.7) ng/L, the levels of OFQ in PPD group were significantly higher than that in the control group (P < 0.01). (2) The levels of plasma 5-HT in PPD group and control group were (1.0 +/- 0.3) micro mol/L and (1.4 +/- 0.4) micro mol/L respectively, the levels of 5-HT in PPD group decreased significantly (P < 0.05). (3) In the PPD group, there was a significant negative correlation between the OFQ and 5-HT level (P < 0.05). CONCLUSION: The PPD was associated with OFQ and 5-HT, the changes of OFQ levels may play an important role in the pathogenesis of the PPD.

[Changes of hypothalamus and peripheral orphanin in fetal rats with intrauterine ischemia and hypoxia].

OBJECTIVE: To evaluate the role of orphanin in the perinatal ischemia-hypoxia. METHODS: The concentration of hypothalamus and peripheral orphanin were measured by radioimmunoassay. Animal model of perinatal ischemia-hypoxia was set up by ligating uterine vessels. All the rats were delivered by cesarean section and scored according to respiration, heart beat, skin color, muscle tone and reflex after delivery. RESULTS: (1) The levels of orphanin in hypothalamus and peripheral blood in group B were (114 +/- 21) pg/g and (58 +/- 11) ng/L respectively. In group A, the were (71 +/- 14) pg/g and (31 +/- 7) ng/L respectively, the levels of orphanin in group B increased significantly when compared with the group A (P < 0.05). In control group, the levels of orphanin were (48 +/- 9) pg/g and (19 +/- 4) ng/L. The levels of orphanin in group A and B were significantly higher than those in the control group (P < 0.01, P < 0.05). (2) The Apgar scores in groups A and B were significantly decreased than that in control group (P < 0.01). The group A pups had significantly better scores than the group B (P < 0.05). CONCLUSION: The perinatal ischemia and hypoxia was associated with orphanin, the changes of orphanin levels may play an important role in the pathophysiological changes in perinatal ischemia and hypoxia.

[Effect of Salvia miltiorrhiza on neuropeptide Y1-36 and calcitonin gene-related peptide in neonatal rats with hypoxia-ischemic brain injury].

OBJECTIVE: To observe the effects of Salvia miltiorrhiza (SM) on levels of neuropeptide Y1-36 and calcitonin gene-related peptide immune reactive substances (ir-NPY, ir-CGRP) in blood plasma and pons-oblongata after hypoxia-ischemic brain injury (HIBI) in neonatal rats. METHODS: Seven-day old rats were randomized into HIBI group (A), HIBI + SM group (B) and sham operation group(C). And each group was subdivided into 4 subgroups according to the different time after operation. 0.5 ml SM was injected intraperitoneally immediately and every 12 hrs afterwards. Changes of ir-NPY and ir-CGRP levels in plasma and pons-oblongata were observed immediately and 12, 24 and 48 hrs after HIBI by radioimmunoassay. RESULTS: Plasma levels of ir-NPY and ir-CGRP in different times after HIBI were all significantly raised but those in pons-oblongata were either raised or lowered to a certain degree. Part of the elevated ir-NPY could be reversed by SM injection. CONCLUSION: Central and peripheral neuropeptide Y1-36 and calcitonin gene-related peptide take part in the pathophysiological process of HIBI, SM could partially reverse the abnormal post-HIBI elevation of ir-NPY, which may be one of the pathways of SM in promoting recovery of damaged brain function.