scholarly journals Generational sensitivity alteration in Chironomus yoshimatsui to carbamate and pharmaceutical chemicals and the effect on Catalase, CYP450, and hemoglobin gene transcription

Ecotoxicology ◽  
2021 ◽  
Author(s):  
Makoto Ishimota ◽  
Naruto Tomiyama
2021 ◽  
Author(s):  
Makoto Ishimota ◽  
Naruto Tomiyama

Abstract To ascertain the tolerance mechanisms of aquatic organisms to artificial chemicals, intergenerational sensitivity changes of Chironomus yoshimatsui to a carbamate pesticide (pirimicarb) and pharmaceutical chemical (diazepam) were investigated. The larvae (< 48-h-old) in each generation were exposed to both chemicals for 48 h and then the surviving chironomids were cultured until the fifth generation (F0–F4) without chemical addition. The 48-h 50% effective concentration (EC50) value of chironomids was determined for each generation. In the pirimicarb treatment group, the EC50 values significantly increased in F3 and F4, and those in the diazepam treatment group slightly increased. Catalase, Cytochrome P450 and hemoglobin (Hb) mRNA levels were monitored to see whether these were related to the trans-generational sensitivity. Although the generalized linear model results showed that the sensitivity to diazepam was slightly increased in the diazepam treatment, we could not find any mRNA levels related to sensitivity alteration. In contrast, the model approach showed that the chironomids exposed to pirimicarb trans-generationally became tolerant with increasing Hb mRNA levels. Therefore, they might decrease their oxidative chemical stress by modifying Hb gene transcription.


2001 ◽  
Vol 268 (6) ◽  
pp. 1802-1810
Author(s):  
Danielle Naville ◽  
Estelle Bordet ◽  
Marie-Claude Berthelon ◽  
Philippe Durand ◽  
Martine Begeot

2001 ◽  
Vol 61 (7) ◽  
pp. 61-67 ◽  
Author(s):  
Thomas V. O. Hansen ◽  
Finn C. Nielsen
Keyword(s):  

Virology ◽  
1988 ◽  
Vol 167 (2) ◽  
pp. 568-577 ◽  
Author(s):  
D DANIELS ◽  
M SUBBARAO ◽  
F BLATTNER ◽  
H LOZERON

1972 ◽  
Vol 71 (2_Suppla) ◽  
pp. S346-S368 ◽  
Author(s):  
Roger W. Turkington ◽  
Nobuyuki Kadohama

ABSTRACT Hormonal activation of gene transcription has been studied in a model system, the mouse mammary gland in organ culture. Transcriptive activity is stimulated in mammary stem cells by insulin, and in mammary alveolar cells by prolactin and insulin. Studies on the template requirement for expression of the genes for milk proteins demonstrate that DNA methylation has an obligatory dependence upon DNA synthesis, but is otherwise independent from hormonal regulation of mammary cell differentiation. Incorporation of 5-bromo-2′deoxyuridine into DNA selectively inhibits expression of the genes for specific milk proteins. Undifferentiated mammary cells activate the synthesis of specific acidic nuclear proteins when stimulated by insulin. Several of these induced acidic nuclear proteins are undetectable in unstimulated undifferentiated cells, but appear to be characteristic components of the nuclei of differentiated cells. These results indicate that mammary cell differentiation is associated with a change in acidic nuclear proteins, and they provide evidence to support the concept that acidic nuclear proteins may be involved in the regulation of gene transcription and of mammary cell differentiation.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2160-P
Author(s):  
ANAND HARDIKAR ◽  
WILSON WONG ◽  
MUGDHA JOGLEKAR ◽  
LOUISE T. DALGAARD ◽  
ALICIA JENKINS ◽  
...  

2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.


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