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Copyright of Journal of Agricultural Science & Technology (1008-0864) is the property of Journal of Agricultural Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To analyze the contribution and interaction of polycyclic aromatic hydrocarbons (PAH)-DNA adducts and changes of telomere length (TL) on missed abortion. Methods: From March to December 2019, patients with missed abortion in the First Hospital of Shanxi Medical University and pregnant women with normal pregnancy but voluntary abortion in the same department during the same period were selected and divided into a case group and a control group. Questionnaire was used to investigate the general situation and the pregnancy situation of the subjects. The abortion villi were collected and the content of PAH-DNA adducts and TL was detected. Logistic regression model was used to analyze the associated factors of missed abortion. R epiR package and Mediation package were used to analyze the effect and relationship between PAH-DNA adducts and TL on missed abortion. Results: The age of the subjects was(29.92±5.69)years old. The M ( Q 1 )of PAH-DNA adducts was 453.75(404.61, 504.72) pg/ml. The Q 3 )of PAH-DNA adducts was 453.75(404.61, 504.72) pg/ml. The M )of TL was 1.21(0.77, 1.72). The content of PAH-DNA adducts in the case group was higher than that in the control group ( Q 1 , Q 3 )of TL was 1.21(0.77, 1.72). The content of PAH-DNA adducts in the case group was higher than that in the control group ( Z <0.001). Multivariate logistic regression showed that low, medium and high levels of PAH-DNA adducts ( P =0.036), while the TL was lower than that in the control group ( Z =-4.05, P <0.001). Multivariate logistic regression showed that low, medium and high levels of PAH-DNA adducts ( OR =3.17,95% CI :1.41-7.14; OR =2.85,95% CI :1.25-6.52; OR =2.46,95% CI :1.07-5.64), and long, medium and short levels of TL ( OR =2.50,95% CI :1.11-5.63; OR :1.42-7.26) were all risk factors for missed abortion. The medium level of PAH-DNA adducts had a 2.76-fold higher risk of shortened TL than those with the lowest level, and no mediating role of TL was found. The stratified analysis showed that when the TL level was longer (>1.21), the low and high levels of PAH-DNA adducts were associated with missed abortion (all CI <0.05); when the TL level was shorter (<1.21), the medium level of PAH-DNA adducts was associated with abortion ( OR =0.025). At lower levels of PAH-DNA adducts, no effect of TL on missed abortion was observed, while, at higher levels, TL was strongly associated with missed abortion ( CI :1.42-7.26) were all risk factors for missed abortion. The medium level of PAH-DNA adducts had a 2.76-fold higher risk of shortened TL than those with the lowest level, and no mediating role of TL was found. The stratified analysis showed that when the TL level was longer (>1.21), the low and high levels of PAH-DNA adducts were associated with missed abortion (all P <0.05); when the TL level was shorter (<1.21), the medium level of PAH-DNA adducts was associated with abortion ( P =0.025). At lower levels of PAH-DNA adducts, no effect of TL on missed abortion was observed, while, at higher levels, TL was strongly associated with missed abortion ( OR =7.50,95% CI :1.95-28.82; OR =6.04,95% CI :1.54-23.65; OR =9.05,95% CI :2.34-35.04). The interaction analysis found that the AP was 0.72 (95% CI The high level of PAH-DNA adducts and shortened TL may increase the risk of missed abortion, and there may be a positive additive interaction between the two factors on missed abortion.SI was 5.21 (95% CI : 2.30-11.77). Conclusion: The high level of PAH-DNA adducts and shortened TL may increase the risk of missed abortion, and there may be a positive additive interaction between the two factors on missed abortion.

Objective: To explore the effects of mothers' exposure to polycyclic aromatic hydrocarbons during pregnancy on their children's neurobehavioral development. Methods: In November 2009 to April 2010, a total of 221 pairs of mother-newborn pairs were recruited from two cooperative hospitals in Taiyuan, and their children were followed up at age two. High performance liquid chromatography was used to determine the level of BPDE-DNA in cord blood leukocytes. The Neonatal behavioral neurological assessment (NBNA) was used to assess the neurodevelopment of newborns, and the Gesell Development Scale was used to measure neurodevelopmental indexes of 2-year-old children. NBNA includes behavior, active and passive tone, primitive reflexes and general assessment, with a total score of 40 points. The Gesell Developmental Schedules consisted of four sub-scales: motor development, adaptive behavior development, language development and personal-social behavior development. We used mean and standard deviation to describe continuous variables with normal distribution, median (interquartile range) to describe continuous variables with skewed distribution, and frequency and proportion to describe categorical variables. Restricted cubic spline models were applied to assess the dose-response relationships between maternal prenatal polycyclic aromatic hydrocarbons exposure and children's neurobehavioral development at two years old. Generalized linear models were applied to evaluate the effect of exposure to maternal prenatal polycyclic aromatic hydrocarbons exposure on children's neurobehavioral development at 0 and two years old. Results: The NBNA score was 38.0±0.8, and the scores of 2-year-old children's motor, adaptive, language and personal-social were 111.6±15.0, 110.5±14.6, 108.8±17.2 and 111.7±14.5, respectively. After adjusting for confounding factors, there is no dose-response association between the cord blood BPDE of pregnant women and neonatal NBNA scores, but there were dose-response associations between BPDE and scores of 2-year-old children's motor, adaptive, language and personal-social. A unit increase in cord blood ln (BPDE-DNA), the score of motor, adaptive, language and personal-social of 2-year-old children decreased on average by 4.54、6.29、8.41 and 7.02 points. Conclusion: Maternal exposure to polycyclic aromatic hydrocarbons during pregnancy is associated with decreased children's neurobehavioral development at two years old.

Objective: To investigate the dose-response relationship between serum polycyclic aromatic hydrocarbon adducts and serum complement C3 and C4 levels among children from a city in East China. Methods: In September 2016, two boarding schools in the air pollution exposure area and the control area (beyond the upwind of 30 km in the air pollution exposure area) in a city in East China were selected as the research site, and the eligible school-age children were recruited as the research objects. A total of 273 children were included, including 163 in the exposure group and 110 in the control group. The annual air pollutant data (PM 2.5 , PM 10 and NO 2 ) of the two regions during the study period were collected. The exposure level of tobacco was evaluated by cotinine in urine. The levels of serum complement C3 and C4 were determined by automatic biochemical analyzer. The serum anti-7, 8, -dihydrodiol-9, 10-epoxide benzo[a]pyrene (BPDE)-albumin adduct levels were detected by ELISA. Linear regression model was used to explore the dose-response relationship between BPDE-albumin adducts and serum complement C3 and C4. Results: The age of 273 subjects was (13.67±0.37) years old, including 165 boys (60.4%). The average annual exposure levels of PM 2.5 , PM 10 and NO 2 and the level of serum BPDE-albumin adducts in the exposure group were higher than those in the control group ( P <0.05). The results of linear regression model analysis showed that after adjusting age, sex, BMI z-score and urinary cotinine level, when the serum BPDE-albumin adduct level increased by 10%, the serum complement C4 level decreased by 1.2% ( P =0.017). After adjusting age, BMI z-score and urinary cotinine level, for every 10% increase in serum BPDE-albumin adduct level in boys, the serum complement C4 level decreased by 1.68% ( P =0.024). After adjusting age, sex and BMI z-score, the levels of serum complement C3 and C4 decreased by 1.31% and 3.57% respectively for every 10% increase in serum BPDE-albumin adducts among children in the urinary cotinine detection group ( P <0.05). Conclusion: There is a significant dose-response relationship between serum BPDE-albumin adducts and the complement C4 among children.

This study aims to establish a quantitative method of 4 aristolochic acids-DNA adducts in mice kidney and liver based on high performance liquid chromatography-tandem mass spectrometry(HPLC-MS/MS) for monitoring the content changes of aristolochic acids-DNA adducts. A Shiseido Capcellpak AQ C&#95;(18) column(3 mm×100 mm, 3 μm) was used, with a mixture of 0.2% acetic acid-5 mmol·L~(-1) ammonium acetate as the aqueous phase and methanol as the organic phase for gradient elution. The multiple reaction monitoring(MRM) scanning method under positive mode by electrospray ionization(ESI) was performed for the detection of the aristolochic acids-DNA adducts which formed by combining aristolochic acid Ⅰ/Ⅱ with deoxyadenosine, deoxyguanosine, and deoxycytidine, respectively. Balb/c mice were given Guanmutong extract by gavage, and the relative content of aristolochic acids-DNA adducts in liver and kidney samples were analyzed within 60 days. It was found that the concentration of 4 aristolochic acids-DNA adducts in the kidney was significantly higher than that in the liver, and there were about 15.87 adducts in per 1×10~6 normal deoxynucleosides, which was 4.5-7.5 times than that of the liver. What's more, some adducts can still be detected on the 30 th day after administration. The concentration of the adducts in the liver was highest on the first day after administration, and a second peak appeared during the 7 th to 14 th days. The results indicated that aristolochic acids-DNA adducts are difficult to eliminate in vivo, and it is of great significance to study the mechanism of liver and kidney injury of aristolochic acid.

Objective: To establish a mouse lung cancer model induced by benzo[a]pyrene(B[a]P) dynamic inhalation exposure., Methods: A total of 96 C57 BL/6 J mice weighing 18 to 20 g were randomly divided into the control group(n=48)and the experimental group(n=48), male and female in half. The experimental group was treated with 10. 0 μg/m~3 BaP for 13 weeks or 25 weeks(6 h per day and 5 days per week) by dynamic inhalation exposure, while the control group was given dimethyl sulfoxide(DMSO). The 13 weeks or 25 weeks after B[a]P exposure, 24 mice were sacrificed and their lung tissues dissected and observed for tumor formation. During B[a]P exposure, the gas in the poisoning cabinet was collected by the active carbon tube method regularly, and the concentration of B[a]P in the poisoning cabinet was analyzed by gas chromatography mass spectrometer, and the(7 R, 8 S)-dihydroxy-(9 S, 10 R)-epoxy-7, 8, 9, 10-tetrahydrobenzo [a] pyrene(BPDE)-DNA adduct content in the whole blood of mice was determined by ELISA., Results: Concentration of B[a]P in the dynamic inhalation cabinet was stable at(12. 794±0. 518)μg/m~3. There was no significant difference in the BPDE-DNA content in the experimental objects between 13 weeks and 25 weeks after B[a]P exposure(P&gt;0. 05). After 25 weeks of B[a]P exposure, the lung cancer formation rate in the experimental group was significantly higher than that in the control group(P&lt;0. 05), the tumor formation rate of female mice was up to 100%., Conclusion: The mice lung cancer model induced by B[a]P dynamic inhalation exposure was established successfully.

Objective: To find out a method to determine the pyrrole adducts in the hairs. Methods: Collected the hair from common people and rats, defatted after completely washed, steeped the hair in different concentration of 2, 5 - hexandione to build hair model containing pyrrole adducts; dissolved the hair and determined the concentration of pyrrole adducts. Results: (1) . The combination of 0.72 mol/L of sodium hydrate and 2% tyrisin could dissolve the hair, and the digestion liquid could react with the Ehrlich's reagent showing fuchsia color; (2) . The color could maintain longer after adding more ethanol; (3) . More pyrrole adducts would be produced by the increasing the concentration of 2, 5-dihexandione ( P <0.01) ; (4) . Concentration of pyrrole adducts in n-hexane treated hair showed no difference compared with control ( P >0.05) . Conclusion: the method could be used to determine the concentration of pyrrole adducts in hair exposed to n - hexane.

Objective: To investigate the association between etheno-DNA adduct and the promoter of DNA methylation levels of cyclin dependent kinase inhibitor 2A (P16), Ras association domain family 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in workers with occupational exposure to diesel engine exhaust (DEE). Methods: We recruited 124 diesel engine testing workers as DEE exposure group and 112 water pump operator in the same area as control group in Henan province in 2012 using cluster sampling. The demographic data were obtained by questionnaire survey; urine after work and venous blood samples were collected from each subject. The urinary etheno-DNA adducts were detected using UPLC-MS/MS, including 1,N6-etheno-2'-deoxyadenosine (εdA) and 3,N4-etheno-2'-deoxycytidine(εdC). The DNA methylation levels of P16, RASSF1A, and MGMT were evaluated using bisulfite-pyrosequencing assay. The percentage of methylation was expressed as the 5-methylcytosine (5mC) over the sum of cytosines (%5mC). Spearman correlation and multiple linear regression were applied to analyze the association between etheno-DNA adducts and DNA methylation of P16, RASSF1A, and MGMT. Results: The median ( P (25)- P (75)) of urinary εdA level was 230.00 (98.04-470.91) pmol/g creatinine in DEE exposure group, and 102.10 (49.95-194.48) creatinine in control group. The level of εdA was higher in DEE exposure group than control group ( P< 0.001). DNA methylation levels of P16, RASSF1A and MGMT were 2.04±0.41, 2.19 (1.94-2.51), 2.22 (1.94-2.46)%5mC in exposure group, and 2.19±0.40, 2.41 (2.11-2.67), 2.44 (2.15-2.91)%5mC in control group. DNA methylation levels were lower in exposure group ( P values were 0.005, 0.002 and 0.001, respectively). Spearman correlation analysis showed that DNA methylation levels of P16, RASSF1A, and MGMT were negative associated with urinary εdA level ( r values were -0.155, -0.137, and -0.198, respectively, P< 0.05). No significant correlation was observed between the εdC level and any measured DNA methylation levels ( P> 0.05) . Multiple linear regression confirmed the negative correlation between εdA and DNA methylation levels of P16, RASSF1A, and MGMT in non-smoking group (β (95 %CI ) was -0.068 (-0.132--0.003), -0.082 (-0.159--0.004) and -0.048 (-0.090--0.007), P values were 0.039, 0.039 and 0.024, respectively). Moreover, εdC was negative associated with DNA methylation level of MGMT in non-smoking group (β (95 %CI ) was -0.094 (-0.179--0.008), P= 0.032). Conclusion: DEE exposure could induce the increased of εdA and decreased of DNA methylation levels of P16, RASSF1A and MGMT.

Objective: To explore the relationship of GSTT1, GSTM1 gene polymorphisms and PAH-DNA adduct with pathogenesis of multiple myeloma., Methods: The bone marrow samples from 37 newly-diagnosed MM patients and 52 healthy peoples as controls were collected; the PCR-based restriction fragment length polymorphism (PCR-RFLP) method was used to detecte the polymorphism of GSTT1 and GSTM1, and to analysis their relationship with clinical characters of MM patients; the engyme linked immunosorbent assay (ELISA) was performed to detect the concentration of PAH-DNA adducts., Results: GSTT1 null and GSTM1 null genotypes increased the risk of multiple myeloma with OR 2.57 (P=0.035) and 1.37 (P>0.05) respectively. In MM patients group, GSTT1 null genotype in stage III was significantly higher than that in stages I, II (P=0.038). However, no statistically significant association was found between GSTT1 gene polymorphism and clinical characters, such as age, type, hemoglobin, β2-MG, albumin. Compared with Hb≥85 g/L of the newly-diagnosed MM patients, MM patients with Hb<85 g/L had significantly higher incidence of GSTM1 null genetype (P<0.05). The level of PAH-DNA adducts in MM patients was higher than that in controls (2358±1182 pg/ml vs 1853±996 pg/ml) (P<0.05). GSTT1 null genotype with PAH-DNA level≥2100 pg/ml showed a risk index of MM (OR=4.500, P<0.05)., Conclusion: GSTT1 gene may have a critical function in the development of MM, and correlates with staging of MM. GSTM1 gene polymorphism correlates with hemoglobin levels of patients with MM. The content of PAH-DNA adducts may play an important role in the pathogenesis of multiple myeloma.

Objective: To study albumin adduct with naphthalene metabolites, namely 1,2-naphthoquinone (1,2-NPQ) and 1,4-naphthoquinone (1,4-NPQ), as a potential biomarker for intermediate/long-term exposure to polycyclic aromatic hydrocarbons (PAH) in coke oven workers., Methods: Twenty-eight coke oven workers and 22 control workers were recruited from a cokery. Spot urine and venous blood samples were collected from the workers after four continuously working days and personal information was obtained by questionnaire. Plasma albumin adduct was detected with gas chromatography-mass spectrometry., Results: Albumin adduct with 1,2- & 1,4-NPQ (1,2-NPQ and 1,4-NPQ), respectively, were detected in all coke oven workers and controls. Median plasma level of 1,2-NPQ-Alb in coke oven workers was significantly higher than that in controls (76.6 pmol/g vs. 44.9 pmol/g, P < 0.01). However, there was no significant difference in plasma median level of 1,4-NPQ-Alb between the two groups (48.6 pmol/g vs. 44.2 pmol/g, P > 0.05). Plasma level of 1,2-NPQ-Alb was significantly higher than that of 1,4-NPQ-Alb in coke oven workers. Urine levels of naphthalene, 1-naphthol, 2-naphthol and 1-pyrenol in coke oven workers correlated significantly with their plasma level of 1,2-NPQ-Alb (Pearson coefficient of correlation greater than 0.371, P < 0.01), but did not do significantly with 1,4-NPQ-Alb., Conclusion: Plasma level of 1,2-NPQ-Alb could effectively reflect their magnitude of personal internal dose of exposure to air PAH, so it could be used as a potential biomarker to evaluate their intermediate/long-term exposure to PAH in coke oven workers.

In order to use the technique of Randomized Terminal Linker-dependent PCR(RDPCR) to detect DNA lesions of specific gene in vivo, rats were administered with potassium dichromate by i.p. injection and genomic DNA of lung were extracted. Single-stranded products were made by repeated primer extension, these products were ligated to a linker and thus amplified by primer P2 and PL. The final PCR products were detected by electrophoresis and Southern hybridization with DIG-labeled probe. The results showed that two hybridization bands for extron 7 of p53 gene were found with dosage of 20.0 mg/kg and 40.0 mg/kg indicating the DNA lesions of extron 7 of p53 gene, by potassium dichromate and there were two DNA lesion cites. The findings from this study provide evidences both for further investigation of mutational mechanism of hexavalent chromium and expansion on using RDPCR in toxicology.

Objective: To study whether the main malondialdehyde-DNA adduct (M1-dG) produced by lipid peroxidation is involved in the carcinogenesis of esophagus., Methods: DNA samples were isolated from normal esophageal epithelium (n = 32) obtained by biopsy and esophageal squamous cell carcinoma specimens (n = 30) obtained by surgery. All tissue samples came from individuals living in Linxian, Henan, a high-risk area of esophageal cancer. Contents of M1-dG adducts were detected by 32P-postlabeling method., Results: M1-dG adducts were detectable both in the normal and cancerous tissue samples. However, normal esophageal epithelial tissues exhibited significantly lower levels of M1-dG adducts (median 3.4, range 1.7/10(8)-55.4/10(8) nucleotides) than those found in esophageal cancer tissues (median 14.1, range 1.4/10(8)-59.0/10(8) nucleotides, P < 0.0001). The adduct levels were neither associated with gender, age, tobacco smoking status or genetic polymorphism in the CYP2E1, an enzyme participating in the oxidation of ethanol to form reactive free radicals., Conclusions: Our findings provide evidence that DNA damage, resulted from lipid peroxidation, can accumulate in the normal human esophageal tissue and reach relatively high level in cancer tissue which suggests that M1-dG adducts may be involved in the initiation and progression of cancer with its mutagenic and carcinogenic effects.

In this paper, a method to determine O6-methylguanine in urine by high performance capillary zone electrophoresis has been established. O6-methylguanine was directly introduced into the capillary employing sodium borate at pH 9.0 as buffer. The capillary used was 75 microns i.d. x 57 cm. The calibration curve showed good linearity, r = 0.9987, CVs were 1.51% for intra-day and 1.93% for inter-day. The average recovery was 98.2%. In conclusion, this method is a simple, rapid, precise and reliable technique for O6-methylguanine measurement in urine.

AFB1 is one of the most potent carcinogenic mycotoxins, naturally occurred in foods. We applied a new SV40-based shuttle vector pSP189 and African Green kidney cells (VeroE6 cell line), which constitute shuttle vector/mammalian cell system to detect mutagenesis induced by AFB1 and to study the effects of AFB1 on the mutation site, type and sequence specificity of DNA molecular level through sequence analysis of pSP189 target gene SupF TRNA. The results indicated that through various time treatment of AFB1 and rat liver microsome, the mutants were obtained by transformation of E. Coli MBM 7070 with progeny of pSP189 generated during replication in veroE6 cells, which increased gradually with the lapse of time, and this experiment showed a significant dose-response relationship. Most detected mutants were point mutations evidenced by agarose gel electrophoresis analysis. The results of direct sequencing SupF TRNA of 53 independent mutants showed that most mutations (about 84.9%) were single base substitutions, among which 95.2% of base substitutions happened on the site of G:C base pair, the predominant mutation was G:C-->T:A transversion, accounting for 53.3%, followed by G:C-->A:T transition, accounting for 35.6%. AFB1-induced mutations did not distributed randomly, and had mutation hot spots and sequence specificity, which contained 5 base pair sequence 5'-NNTTC-3'. The mutations on the SupF shuttle vector were consistent with the results from studies of oncogene tumor suppressor genes and DNA adduct.

Objective: To explore the mechanism of cisplatin resistance and its reversion in human ovarian cancer., Methods: A xenografted cisplatin resistant mice model of human ovarian cancer, SKOV3/cp, was developed by the microencapsulated technique. The multiple changes of bio-chemical markers in the model were determined, and various modulators for reversion were tested., Results: Intracellular platinum accumulation in SKOV3 was 5.1 times, Pt-DNA adducts 2.4 times and interstrand cross link of DNA (ISC) 4.8 times of those in cisplatin-resistant cell line, SKOV3/cp. These changes in SKOV3/cp could not be reversed by verapamil. Amphotercin B (AmB) and Novobiocin (NVB) could raise the concentrations of platinum and Pt-DNA adducts in SKOV3/cp, resulting in complete or partial reversion of cisplatin-resistance of SKOV3/cp. There were no differences in total glutathione (GSH) level and in sensitivity to CdCl2 between SKOV3 and SKOV3/cp., Conclusions: It is suggested that the primary factor causing SKOV3/cp resistance to cisplatin is the reduction of intracellular platinum accumulation and the augmentation of the ability to remove Pt-DNA adducts. The resistance is not considered to be associated with the multidrug resistant, GSH, metallothionein systems. AmB and NVB can overcome cisplatin resistance of SKOV3/cp in vitro and in vivo.

We have compared in vitro binding of adriamycin (ADR) and amsacrine (AMSA) with DNA, the toxicity, and the antitumor activity of ADR-DNA and AMSA-DNA, after intraperitoneal (ip) injection in mice. The binding of ADR with DNA is 100-fold higher than that of AMSA with DNA. The overall toxicity of ADR-DNA is significantly lower than that of ADR. ADR-DNA is more effective than ADR against three models of S180 sarcoma (by sc, ip and i.v. inoculation into mice). The peak levels of ADR-DNA and ADR were 265 +/- 24 ng.ml-1 versus 108 +/- 16 ng.ml-1 (P < 0.01). AUC 0-12 h were 1064 +/- 84 ng.h-1 x ml-1 versus 382 +/- 27 ng.h-1 x ml-1 (P < 0.01). The levels of ADR in most of tissues and tumor after administration of ADR-DNA were higher than those after administration of ADR. Moreover, there is no difference in toxicity, therapeutic effects as well as AUC between AMSA-DNA and AMSA.