scholarly journals LED-phototherapy does not induce oxidative DNA damage in hyperbilirubinemic Gunn rats

2019 ◽  
Vol 85 (7) ◽  
pp. 1041-1047 ◽  
Author(s):  
Lori W. E. van der Schoor ◽  
Christian V. Hulzebos ◽  
Martijn H. van Faassen ◽  
Ido P. Kema ◽  
Alain de Bruin ◽  
...  
Author(s):  
Lori W E van der Schoor ◽  
Martijn H J R van Faassen ◽  
Ido Kema ◽  
Dyvonne H Baptist ◽  
Annelies J Olthuis ◽  
...  

BackgroundPhototherapy is used on the majority of preterm infants with unconjugated hyperbilirubinaemia. The use of fluorescent tube phototherapy is known to induce oxidative DNA damage in infants and has largely been replaced by blue light-emitting diode phototherapy (BLP). To date, it is unknown whether BLP also induces oxidative DNA damage in preterm infants.ObjectiveTo determine whether BLP in preterm infants induces oxidative DNA damage as indicated by 8-hydroxy-2′deoxyguanosine (8-OHdG).DesignObservational cohort study.MethodsUrine samples (n=481) were collected in a cohort of 40 preterm infants (24–32 weeks’ gestational age) during the first week after birth. Urine was analysed for the oxidative marker of DNA damage 8-OHdG and for creatinine, and the 8-OHdG/creatinine ratio was calculated. Durations of phototherapy and levels of irradiance were monitored as well as total serum bilirubin concentrations.ResultsBLP did not alter urinary 8-OHdG/creatinine ratios (B=0.2, 95% CI −6.2 to 6.6) at either low (10–30 µW/cm2/nm) or high (>30 µW/cm2/nm) irradiance: (B=2.3, 95% CI −5.7 to 10.2 and B=−3.0, 95% CI −11.7 to 5.6, respectively). Also, the 8-OHdG/creatinine ratios were independent on phototherapy duration (B=−0.1, 95% CI −0.3 to 0.1).ConclusionsBLP at irradiances up to 35 µW/cm2/nm given to preterm infants ≤32 weeks’ gestation does not affect 8-OHdG, an oxidative marker of DNA damage.


2020 ◽  
Author(s):  
Bin Wang ◽  
Weihong Qiu ◽  
Shijie Yang ◽  
Limin Cao ◽  
Chunmei Zhu ◽  
...  

<a><b>OBJECTIVE: </b></a>Acrylamide exposure from daily-consumed food has raised global concern.<b> </b>We aimed to assess the exposure-response relationships of internal acrylamide exposure with oxidative DNA damage, lipid peroxidation and fasting plasma glucose (FPG) alteration, and investigate the mediating role of oxidative DNA damage and lipid peroxidation in the association of internal acrylamide exposure with FPG. <p><b>RESEARCH DESIGN AND METHODS:</b> FPG and urinary biomarkers of oxidative DNA damage (8-hydroxy-deoxy-guanosine, 8-OHdG), lipid peroxidation (8-iso-prostaglandin-F2α, 8-iso-PGF2α) and acrylamide exposure (N-acetyl-S-(2-carbamoylethyl)-L-cysteine, AAMA; N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine, GAMA) were measured for 3,270 general adults from the Wuhan-Zhuhai cohort. The associations of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG were assessed by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α were evaluated by mediation analysis.</p> <p><b>RESULTS:</b> We found significant linear positive dose-response relationships of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG (except GAMA with FPG), and 8-iso-PGF2α with FPG. Each 1-unit increase in log-transformed level of AAMA, ΣUAAM (AAMA+GAMA) or 8-iso-PGF2α was associated with a 0.17-, 0.15- or 0.23-mmol/L increase in FPG, respectively (<i>P </i>or/and<i> P trend</i><0.05). Each 1% increase in AAMA, GAMA or ΣUAAM was associated with a 0.19%, 0.27% or 0.22% increase in 8-OHdG, respectively, and a 0.40%, 0.48% or 0.44% increase in 8-iso-PGF2α, respectively (<i>P </i>and<i> P trend</i><0.05). Increased 8-iso-PGF2α rather than 8-OHdG significantly mediated 64.29% and 76.92% of the AAMA and ΣUAAM associated-FPG increases, respectively.</p> <p><b>CONCLUSIONS:</b> Exposure of general adult population to acrylamide was associated with FPG elevation, oxidative DNA damage and lipid peroxidation, which in turn partly mediated acrylamide-associated FPG elevation.<b></b></p>


Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.


2012 ◽  
Vol 37 (4) ◽  
pp. 440-448 ◽  
Author(s):  
TRISHNA DEBNATH ◽  
HAI LAN JIN ◽  
MD ABUL HASNAT ◽  
YUNSUK KIM ◽  
NADIRA BINTE SAMAD ◽  
...  

2020 ◽  
pp. 096032712098420
Author(s):  
Ahmet Topal ◽  
Arzu Gergit ◽  
Mustafa Özkaraca

We investigated changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) activity which is a product of oxidative DNA damage, histopathological changes and antioxidant responses in liver and gill tissues of rainbow trout, following a 21-day exposure to three different concentrations of linuron (30 µg/L, 120 µg/L and 240 µg/L). Our results indicated that linuron concentrations caused an increase in LPO levels of liver and gill tissues ( p < 0.05). While linuron induced both increases and decreases in GSH levels and SOD activity, CAT activity was decreased by all concentrations of linuron ( p < 0.05). The immunopositivity of 8-OHdG was detected in the hepatocytes of liver and in the epithelial and chloride cells of the secondary lamellae of the gill tissues. Our results suggested that linuron could cause oxidative DNA damage by causing an increase in 8-OHdG activity in tissues, and it induces histopathological damage and alterations in the antioxidant parameters of the tissues.


DNA Repair ◽  
2021 ◽  
pp. 103117
Author(s):  
Ruikui Zhang ◽  
Tao Wu ◽  
Peipei Zheng ◽  
Ming Liu ◽  
Guixiang Xu ◽  
...  

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