Associations of Urinary Trichloroacetic Acid Concentrations with Spermatozoa Apoptosis and DNA Damage in a Chinese Population

Abstract

Exposure to trichloroacetic acid (TCAA) has been associated with impaired semen quality; however, its association with spermatozoa apoptosis and DNA damage remains unclear. We, therefore, collected single semen and repeated urine samples from male partners of couples attending a reproductive center, which were measured for spermatozoa apoptosis and DNA damage parameters and TCAA concentrations, respectively. Multivariable linear regression models were used to explore the associations between urinary TCAA concentrations and spermatozoa apoptosis (n = 462) and DNA damage parameters (n = 512). After adjusting for potential confounders, positive dose–response relationships were found between urinary TCAA concentrations and percentage of tail DNA (tail%) and tail-distributed moment (TDM) (both p for trend <0.10). Compared with men in the lowest tertile of urinary TCAA concentrations, men in the highest tertile had a greater tail% and TDM of 6.2% (95% CI: 0.7, 12.2%) and 8.9% (95% CI: −1.9, 20.5%), respectively. Urinary TCAA concentrations were unrelated to spermatozoa apoptosis parameters in a dose–response manner. However, urinary TCAA concentrations were positively associated with the percentage of Annexin V+/PI– spermatozoa (apoptotic cells), when urinary TCAA concentrations were modeled as continuous variables. Our results suggest that exposure to TCAA at concentrations in real-world scenarios may be associated with spermatozoa apoptosis and DNA damage.

Gastrointestinal Degradation and Toxicity of Disinfection Byproducts in Drinking Water Using In Vitro Models and the Roles of Gut Microbiota

“…Previous studies illustrated that the induction of oxidative stress was one of the toxicity mechanisms of DBPs. , The increased levels of 8-OHdG indicated that excessive intracellular ROS triggers DNA damage (Figure c) Figure d shows that DBPs could significantly reduce the normalized JC-1 value in DLD-1 cells, suggesting that DBPs might induce apoptosis at noncytotoxic concentrations triggered by excessive intracellular ROS, which was consistent with previous studies about HANs and HAAs …”

“…42 Figure 2d shows that DBPs could significantly reduce the normalized JC-1 value in DLD-1 cells, suggesting that DBPs might induce apoptosis at noncytotoxic concentrations triggered by excessive intracellular ROS, 43 which was consistent with previous studies about HANs 44 and HAAs. 45 Third, to further investigate the toxicity mechanisms of DBPs, the transcriptomic profiles of DLD-1 cells were analyzed based on RNA-Seq after DBP exposure with EC 0 values, and detailed sequencing data information is provided in Table S3. Principal coordinate analysis (PCoA) of the transcriptional profiles showed significant separation among the CK group and DBP exposure groups (Figure 2e), indicating that DBPs significantly altered the transcriptome of the DLD-1 cells.…”

Urinary haloacetic acid concentrations in relation to sex and thyroid hormones among reproductive-aged men

“…Given that urinary HAA concentrations varied greatly within a given day and that the collection of repeated urine samples improved exposure estimation ( Wang et al, 2014 ), two urine samples were collected from each man at different time points (mean duration: 4.4 ± 3.7 hrs; range: 2.0–10.6 hrs) on their visiting day to the clinic. The samples were stored at −40°C and analyzed for urinary concentrations of DCAA, TCAA, and creatinine using a procedure described in our previous studies ( Chen et al, 2022 ; Wang et al, 2019 ). The limit of detection (LOD) of the gas chromatograph (GC) for DCAA and TCAA was 1.0 and 0.5 μg/L, respectively.…”

“…Dichloroacetic acid (DCAA) and trichloroacetic acid (TCAA) are two leading species of HAAs; their excretions, particularly TCAA in urine samples, have been strongly associated with ingested trihalomethanes (THMs) and HAAs ( Kim et al, 1999 ; Weisel et al, 1999 ). Therefore, they are proposed as reliable exposure markers for ingested DBPs in drinking water ( Kim et al, 1999 ; Wang et al, 2014 ; Chen et al, 2022 ; Sun et al, 2020 ).…”

Oxidative Stress Biomarkers in Male Infertility: Established Methodologies and Future Perspectives

“…Insecticides, pesticides, and environmental toxins (heavy metals, bisphenol A, and dioxins) lead to a reduction in male fertility, causing an alteration in sperm DNA both directly and indirectly, through the production of ROS, with a consequent reduction in the number of ejaculated spermatozoa and the presence of morphologically abnormal spermatozoa in seminal fluid [8][9][10][11][12]. Associations have also been found between the urinary concentrations of particular oxidative substances and sperm apoptosis [13,14].…”