Maintaining telomere length plays a crucial role in regulating cellular life span. Telomere lengthening or shortening is one of the important biomarkers which could predict the preceding or present diseases. Meanwhile, the impact of environmental arsenic exposure on telomere length has increasingly concerned. Although previous studies demonstrated the effects of arsenic on telomere length, the findings were unclear on whether telomere shortens or lengthens by arsenic exposure. Thus, this manuscript summarized and discussed the telomere length alteration following arsenic exposure and the possible does-response effect of arsenic on telomere length. The present review suggested that different age groups may respond differently to arsenic exposure, and the dose-response effect of arsenic could be a critical factor in its effect on telomere length. Moreover, speciation analysis of arsenic could be more informative in identifying the effect of arsenic on telomere length.
Elevated sperm mitochondrial DNA copy number (mtDNAcn) is associated with damage to sperm and poorer measures of semen quality. Exposure to cadmium (Cd) can increase oxidative stress and damage sperm mitochondria. The adverse effects of Cd can potentially be reduced by sufficient selenium (Se). The objective of this study was to examine the associations between sperm mtDNAcn and urinary concentrations of Cd, Se, and the Cd/Se molar ratio. Participants were recruited from patients who sought infertility treatment at two hospitals in Japan. Urine and semen specimens and self-administered questionnaires were collected on the day of recruitment. Sperm mtDNAcn was measured in extracted sperm DNA by multiplex real-time qPCR. Urinary Cd and Se concentrations were measured using inductively coupled plasma mass spectrometry. Cd/Se molar weights were calculated to obtain the molar ratio. Linear regression was used to predict associations after adjusting for age, BMI, smoking, drinking, exercise, varicocele, and hospital of recruitment. Sperm mtDNAcn showed statistically insignificant associations with urinary Cd (β = 0.13, 95% CI -0.18, 0.44), urinary Se concentration (β = -0.09, 95% CI -0.54, 0.35), and Cd/Se molar ratio (β = 0.12, 95% -0.13, 0.37). The current study did not find evidence of urinary Cd or Se concentrations or Cd/Se molar ratio being related to mtDNAcn.
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