There is accumulating epidemiologic evidence that exposure to traffic-related air pollutants, including particulate matter (PM) and polyaromatic hydro carbons (PAHs), plays a role in etiology and prognosis of a large scale of illnesses, although the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown. Our general objective was to assess the relations between personal exposure to traffic exhausts, in particular ambient PM_2.5 and PAHs, and the occurrence of DNA strand breaks by applying personal monitoring of PM and biomarkers of exposure (urinary 1-hydroxypyrene-glucuronide, 1-OHPG) and effect (urinary 8-hydroxydeoxyguanosine, 8-OHdG and DNA strand breaks). We recruited 91 traffic conductors and 53 indoor office workers between May 2009 and June 2011 in Taipei City, Taiwan. We used PM_2.5 personal samplers to collect breathing-zone particulate PAHs samples. Spot urine and blood samples after work shift of 2 consecutive days were analyzed for 1-OHPG, 8-OHdG and DNA strand breaks, respectively. Statistical methods included linear regression and mixed models. Urinary 8-OHdG levels and the occurrence of DNA strand breaks in traffic conductors significantly exceeded those in indoor office workers in mixed models. Particulate PAHs levels showed a positive association with urinary 1-OHPG in the regression model (β = 0.056, p = 0.01). Urinary 1-OHPG levels were significantly associated with urinary 8-OHdG levels in the mixed model (β = 0.101, p = 0.023). Our results provide evidence that exposure to fine particulates causes DNA damage. Further, particulate PAHs could be biologically active constituents of PM_2.5 with reference to the induction of oxidative DNA damages.

Hot water was used to obtain Chlorella sorokiniana hot water extract (HWE). Subsequently, this byproduct was freeze-dried, hydrolysed at 50 °C using Protease N to obtain C. sorokiniana protein hydrolysates (PN-1), and then digested with a gastrointestinal enzyme (PN-1G). The inhibitory effects of the HWE and hydrolysates against angiotensin I-converting enzyme (ACE) were investigated. The soluble protein and peptide contents were 379.9 and 179.7 mg/g, respectively, for HWE and 574.8 and 332.8 mg/g, respectively, for PN-1. The IC₅₀ values of the HWE, PN-1, and PN-1G on ACE were 1.070, 0.035, and 0.044 mg/mL, respectively. PN-1G was separated into seven fractions through size exclusion chromatography. The sixth fraction of the hydrolysate had a molecular weight between 270 and 340 Da, and the lowest IC₅₀ value on ACE was 0.015 mg/mL. The amino acid sequences of the ACE-inhibitory peptides were Trp-Val, Val-Trp, Ile-Trp, and Leu-Trp, of which the IC₅₀ values were 307.61, 0.58, 0.50, and 1.11 µΜ, respectively. Systolic blood pressure and diastolic blood pressure were reduced 20 and 21 mm Hg, respectively, in spontaneously hypertensive rats after 6 h of oral administration with a dose of 171.4 mg PN-1 powder/kg body weight.

This research focuses on cobia skin hydrolysates and their antihypertensive effects via the inhibitory activities of angiotensin I-converting enzyme (ACE). Marine fish Cobia (Rachycentron canadum) skin was hydrolysed for 5 h using Protamex and Protease N to obtain the cobia skin protein hydrolysates PX-5 and PN-5, respectively. The soluble protein and peptide contents of the PX-5 were 612 and 270 mg/g, respectively, and for the PN-5, 531 and 400 mg/g, respectively. The IC₅₀ of PX-5 and PN-5 on ACE was 0.221 and 0.291 mg/mL, respectively. Increasing the IC₅₀ from 0.221 to 0.044 mg/mL by simulated gastrointestinal digestion (PX-5G) reduced the ACE-inhibitory capacity of PX-5. Using gel filtration chromatography, the PX-5G was fractioned into eight fractions. The molecular weight of the fifth fraction from PX-5G was between 630 and 450 Da, and the highest inhibitory efficiency ratio on ACE was 1552.4%/mg/mL. We identified four peptide sequences: Trp-Ala-Ala, Ala-Trp-Trp, Ile-Trp-Trp, and Trp-Leu, with IC₅₀ values for ACE of 118.50, 9.40, 0.51, and 26.80 μM, respectively. At a dose of 600 mg PX-5 powder/kg body weight, in spontaneously hypertensive rats PX-5’s antihypertensive effect significantly reduced systolic and diastolic blood pressure by 21.9 and 15.5 mm Hg, respectively, after 4 h of oral gavage.