This study aims to investigate the mechanisms involved in the action of lutein (LU) alleviating arsenic-induced reproductive toxicity using mice model. Forty male Kunming mice were received following treatments by gavage: normal saline solution (control), arsenic trioxide (ATO; 5 mg/kg/day), LU (40 mg/kg/day), and ATO + LU (5 mg/kg/day + 40 mg/kg/day). At the end, the mice were killed by cervical dislocation and weighed. Pathological examination was done on the testis. The biomedical parameters including superoxide dismutase (SOD), glutathione (GSH), total antioxidative capability, malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), and reproductive indexes were analyzed. The messenger RNA (mRNA) and protein expression of Nrf2, heme oxygenase 1 (HO-1), glutathione S-transferase (GST), nicotinamide adenine dinucleotide phosphate dehydrogenase, quinone 1 (NQO1) in testis were detected by real-time polymerase chain reaction and Western blot. We found that there was a decrease in sperm count; testis somatic index; the activities of SOD, GSH, total antioxidative capacity ( p < 0.01, respectively) in ATO-treated mice, while there was an increase in the levels of sperm abnormalities, MDA, and 8-OHdG than control ( p < 0.01, respectively). The groups treated with ATO + LU showed recovery of the measured parameters between those of ATO or saline-treated group. The antagonized interaction between ATO and LU was statistically significant ( p < 0.01). Mice treated with ATO + LU also showed greater mRNA expression of Nrf2, HO-1, NQO1, and GST than ATO or saline-treated groups. These findings suggest that LU alleviates reproductive toxicity induced by arsenic in male mice via Nrf2 signaling, which implicates a possible mechanism of LU in preventing the reproductive injury, and elucidates that consuming the rich plant sources of LU will alleviate the reproductive toxicity induced by chemicals.

ABSTRACT. The aim of this study was to assess the association between three FTO polymorphisms (rs9939609, rs8057044, and rs1421085) and metabolic syndrome (MS)-related outcomes in the low-income, rural, nomadic minority Khazakh population in far western China. A total of 489 subjects (245 MS patients, 244 controls) were included in the study and DNA samples were genotyped for the three polymorphisms by matrixassisted laser desorption/ionization time of flight mass spectrometry. The frequencies of the rs1421085 and rs9939609 genotypes and alleles did not differ significantly between MS patients and control, while the frequencies of rs8057044 G alleles and GG genotypes were higher in MS patients (P < 0.05) than in control subjects (G: 61.16 vs 53.53%, GG: 39.07 vs 29.05%) and the frequencies of rs8057044 A genotypes and alleles were lower (P < 0.05) in MS patients compared with controls (AA: 17.36 vs 21.99%, A: (2015) 38.84 vs 46.47%). Risk analysis of the rs8057044 polymorphism revealed individuals with GA and GG genotypes to have 1.112 and 1.731 times higher risks of developing MS than those with the AA genotype, respectively, while the G allele was found to be associated with a 1.367 times higher risk of developing MS compared with the A allele. These apparent correlations, however, did not hold true when adjusted for BMI. Weight, WC, HC, and BMI differed significantly between rs8057044 GG and AA+GA genotypes (P < 0.05).

ABSTRACT. We investigated the relationship between haplotype and linkage disequilibrium of the PPARγ gene polymorphisms rs3856806, rs12490265, rs1797912, and rs1175543 and metabolic syndrome (MS) in the Kazakh people of Xinjiang Province. For PPARγ, rs3856806, rs12490265, rs1797912, and rs1175543 genotypes were detected in 489 subjects (including 245 MS patients and 244 controls) using matrixassisted laser desorption-ionization time-of-flight mass spectrometry. Frequencies of rs3856806T, rs12490265A, rs1797912C, and rs1175543G alleles in MS patients were significantly lower than those of controls [rs3856806T allele: 12.53 vs 17.01% (P = 0.044), rs12490265A allele: 31.84 vs 38.52% (P = 0.029), rs1797912C allele: 35.31 vs 43.24% (P = 0.011), rs1175543G allele: 40.61 vs 47.54% (P = 0.029)]. Significant

BackgroundLong-term impact of sepsis on whole body systems is not well investigated. The aim of the study was to explore the potential association of neonatal/adult sepsis with several inflammation-related diseases in multiple physiological systems.MethodsInstrumental variables for neonatal and adult sepsis were collected from the public genome-wide association studies, which must satisfy the correlation, exclusivity and independence assumptions. Mendelian randomization methods (including random-effect inverse-variance weighted, MR-PRESSO, weighted median and MR-Egger) were used to determine the genetic association of neonatal/adult sepsis with asthma, allergy, rheumatoid arthritis, body mass index/obesity, type 1/type 2 diabetes and intelligence/dementia. Sensitivity analyses were conducted to assess heterogeneity and horizontal pleiotropy. The study was performed by TwoSampleMR in R software.ResultsThe inverse-variance weighted method reported that neonatal sepsis was related to the decreased level of body mass index (OR = 0.988, 95%CI = 0.980 ~ 0.997, P = 0.007), and adult sepsis was related to the decreased risk of obesity (OR = 0.785, 95%CI = 0.655 ~ 0.940, P = 0.009). These results were supported by the other Mendelian randomization methods. In addition, the study did not find any association of neonatal/adult sepsis with the other inflammation-related diseases. No heterogeneity and horizontal pleiotropy were found using sensitivity analyses.ConclusionSepsis had the potential to reduce the risk of obesity or body mass index level at a genetic level, both in neonates and in adults.