scholarly journals Impairment of testicular function in adult male Japanese quail (Coturnix japonica) after a single administration of 3-methyl-4-nitrophenol in diesel exhaust particles

2006 ◽  
Vol 189 (3) ◽  
pp. 555-564 ◽  
Author(s):  
Chun-Mei Li ◽  
Shinji Takahashi ◽  
Shinji Taneda ◽  
Chie Furuta ◽  
Gen Watanabe ◽  
...  

The effects of 3-methyl-4-nitrophenol (PNMC), a component of diesel exhaust, on reproductive function were investigated in adult male Japanese quail. The quail were treated with a single i.m. dose of PNMC (78, 103 or 135 mg/kg body weight), and trunk blood and testes were collected 1, 2 or 4 weeks later. Various levels of testicular atrophy were observed in all groups treated with PNMC. Sperm formation, cloacal gland area, and plasma LH and testosterone concentrations were also reduced in birds with testicular atrophy. To determine the acute effect of PNMC on gonadotrophin from the pituitary, adult male quail were administrated a single i.m. injection of PNMC (25 mg/kg), and plasma concentrations of LH were measured at 1, 3 and 6 h. This dose significantly lowered plasma levels of LH at all three time points. These results suggest that PNMC acts on the hypothalamus–pituitary axis, by reducing circulating LH within a few hours of administration and subsequently reducing testosterone secretion. In addition, in order to investigate the direct effects of PNMC on the secretion of testosterone from testicular cells in quail testes, cultured interstitial cells containing Leydig cells were exposed to PNMC (10−6, 10−5 or 10−4 M) for 4, 8 or 24 h. These quantities of PNMC significantly reduced the secretion of testosterone in a time- and dose-dependent manner. The present findings also suggest a direct effect of PNMC on the testis to reduce testosterone secretion. This study clearly indicates that PNMC induces reproductive toxicity at both the central and testicular levels, and disrupts testicular function in adult male quail.

2008 ◽  
Vol 72 (5) ◽  
pp. 1235-1241 ◽  
Author(s):  
Hiromi IZAWA ◽  
Machiko KOHARA ◽  
Koichi AIZAWA ◽  
Hiroyuki SUGANUMA ◽  
Takahiro INAKUMA ◽  
...  

2006 ◽  
Vol 28 (2) ◽  
pp. 252-258 ◽  
Author(s):  
C. Li ◽  
S. Taneda ◽  
A. K. Suzuki ◽  
C. Furuta ◽  
G. Watanabe ◽  
...  

2010 ◽  
Vol 56 (2) ◽  
pp. 195-199 ◽  
Author(s):  
Yuling MI ◽  
Caiqiao ZHANG ◽  
Chun Mei LI ◽  
Shinji TANEDA ◽  
Gen WATANABE ◽  
...  

2019 ◽  
Vol 168 ◽  
pp. 338-347 ◽  
Author(s):  
Mojtaba Ehsanifar ◽  
Abolfazl Azami Tameh ◽  
Mahdi Farzadkia ◽  
Roshanak Rezaei Kalantari ◽  
Mahmood Salami Zavareh ◽  
...  

2009 ◽  
Vol 21 (10) ◽  
pp. 803-811 ◽  
Author(s):  
ChunMei Li ◽  
Shinji Taneda ◽  
Kazuyoshi Taya ◽  
Gen Watanabe ◽  
Xuezheng Li ◽  
...  

1982 ◽  
Vol 92 (2) ◽  
pp. 261-265 ◽  
Author(s):  
O. F. X. ALMEIDA

Adult male Japanese quail held under short daily photoperiods (8 h light: 16 h darkness; 8L : 16D) had significantly higher plasma concentrations of thyroid-stimulating hormone (TSH), tri-iodothyronine (T3) and thyroxine (T4) than did those kept under long days (16L : 8D). When given a single s.c. injection of 50 μg thyrotrophin releasing hormone (TRH) the birds held under both the 8L : 16D and 16L : 8D photoperiods showed rapid increases in their blood concentrations of TSH, T4 and T3, the amplitude of the TSH response of the birds exposed to 16L : 8D being particularly marked. These results suggest that, in the male quail, long daily photoperiods produce a hypothyroid state as a result of diminished TRH secretion. The synthetic and secretory capacities of the thyroid gland and pituitary thyrotrophs are apparently unimpaired by long days.


Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 291
Author(s):  
Joong Won Lee ◽  
Hee Jae Lee ◽  
Young-Joo Lee ◽  
Yong-beom Lim ◽  
Woo Jong Sim ◽  
...  

Several epidemiological studies concluded that inhalation of diesel exhaust particles (DEP) is associated with an increase in the relative risk of lung cancer. In vitro research evaluating the genetic damage and/or changes in gene expression have been attempted to explain the relationship between DEP exposure and carcinogenicity. However, to date, investigations have been largely confined to studies in immortalized or tumorigenic epithelial cell models. Few studies have investigated damage at the chromosomal level to DEP exposure in normal cell lines. Here, we present the genotoxic effects of DEP in normal cells (embryonic human lung fibroblasts) by conventional genotoxicity testing (micronuclei (MN) and comet assay). We show the differentially expressed genes and enriched pathways in DEP-exposed WI-38 cells using RNA sequencing data. We observed a significant increase in single-strand DNA breaks and the frequency of MN in DEP-exposed cells in a dose-dependent manner. The differentially expressed genes following DEP exposure were significantly enriched in the pathway for responding to xenobiotics and DNA damage. Taken together, these results show that DEP exposure induced DNA damage at the chromosomal level in normal human lung cells and provide information on the expression of genes associated with genotoxic stress.


2007 ◽  
Vol 292 (3) ◽  
pp. L664-L670 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Sultan Al-Maskari ◽  
Badreldin H. Ali ◽  
Issa S. Al-Amri

Pollution by particulates has consistently been associated with increased cardiorespiratory morbidity and mortality. It has been suggested that ultrafine particles, of which diesel exhaust particles (DEP) are significant contributors, are able to translocate from the airways into the bloodstream in vivo. In the present study, we assessed the effect of systemic administration of DEP on cardiovascular and respiratory parameters. DEP were administered into the tail vein of rats, and heart rate, blood pressure, blood platelet activation, and lung inflammation were studied 24 h later. Doses of 0.02, 0.1, or 0.5 mg DEP/kg (8, 42, or 212 μg DEP/rat) induced a significant decrease of heart rate and blood pressure compared with saline-treated rats. Although the number of platelets was not affected, all the doses of DEP caused a shortening of the bleeding time. Similarly, in addition to triggering lung edema, the bronchoalveolar lavage analysis revealed the presence of neutrophil influx in DEP-treated rats in a dose-dependent manner. We conclude that the presence of DEP in the systemic circulation leads not only to cardiovascular and haemostatic changes but it also triggers pulmonary inflammation.


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