Nitrite is a common pollutant in water and is highly toxic to aquatic animals. To reveal the mechanism of salinity in attenuating nitrite toxicity to fish, we measured the physiological responses of juvenile Takifugu obscurus exposed to nitrite concentrations (0, 10, 20, 50, and 100 mg/L) under different salinity levels (0, 10, and 20 ppt) for 96 h. Salinity increased the survival rates of juvenile T. obscurus exposed to nitrite. Changes in key hematological parameters, antioxidant system, malondialdehyde, Na⁺/K⁺–ATPase, and HSP70 indicated that nitrite induced considerable damage to juveniles; salinity mitigated the harmful effects. This finding reflects similar changing trends in both antioxidants and their gene expressions among different tissues. We applied an overall index, an integrated biomarker response (IBR), that increased under high−nitrite condition but recovered to the normal levels under salinity treatment. Analysis of the selected detection indices and IBR values showed that the overall mitigating effect of salinity on nitrite toxicity seems to be at sub-cellular level and associated with complicated physiological responses.

The trophic balance of freshwater aquaculture activities has traditionally been monitored by chemical analysis of water; however, the parameters measured are usually characterized by high temporal variability. Aquatic mosses can be used as biomonitors as they integrate both continuous and episodic contamination events. Here we report, for the first time, a method for monitoring N enrichment in the surroundings of fish farms by measuring the N content and isotopic signal (δ15N) of transplanted living and devitalized specimens of the aquatic moss Fontinalis antipyretica. For this purpose, moss samples (“moss bags”) were exposed at increasing distances (10, 100, 300 and 1000 m) up- and downstream of the effluent discharge points of four trout farms, for 10 and 30 days. The low natural (background) variability in δ15N in upstream samples enabled detection of outlier values, caused by aquaculture discharges, at distances of 10 and 100 m downstream, especially in devitalized moss and after 10 days of exposure. However, the unexpectedly low N contents of moss samples exposed close to the discharge points complicates interpretation of the high levels of N forms detected by conventional physicochemical analysis of water. Although the mechanisms that modify N parameters in moss tissues were not clear, measurement of the isotopic signal δ15N in devitalized moss exposed for 10 days proved useful for monitoring the N pollution associated with intensive freshwater aquaculture.

To help understand the pathophysiologic mechanisms linking air pollutants and cardiovascular disease (CVD), we employed a repeated measures design to investigate the associations of four short-term air pollution exposures – particulate matter less than 2.5 μm in diameter (PM₂.₅), nitrogen dioxide (NO₂), ozone (O₃) and sulfur dioxide (SO₂), with two blood markers involved in vascular effects of oxidative stress, soluble lectin-like oxidized LDL receptor-1 (sLOX-1) and nitrite, using data from the Multi-Ethnic Study of Atherosclerosis (MESA). Seven hundred and forty participants with plasma sLOX-1 and nitrite measurements at three exams between 2002 and 2007 were included. Daily PM₂.₅, NO₂, O₃ and SO₂ zero to seven days prior to blood draw were estimated from central monitors in six MESA regions, pre-adjusted using site-specific splines of meteorology and temporal trends, and an indicator for day of the week. Unconstrained distributed lag generalized estimating equations were used to estimate net effects over eight days with adjustment for sociodemographic and behavioral factors. The results showed that higher short-term concentrations of PM₂.₅, but not other pollutants, were associated with increased sLOX-1 analyzed both as a continuous outcome (percent change per interquartile increase: 16.36%, 95%CI: 0.1–35.26%) and dichotomized at the median (odds ratio per interquartile increase: 1.21, 95%CI: 1.01–1.44). The findings were not meaningfully changed after adjustment for additional covariates or in several sensitivity analyses. Pollutant concentrations were not associated with nitrite levels. This study extends earlier experimental findings of increased sLOX-1 levels following PM inhalation to a much larger population and at ambient concentrations. In light of its known mechanistic role in promoting vascular disease, sLOX-1 may be a suitable translational biomarker linking air pollutant exposures and cardiovascular outcomes.

Ocean acidification (OA) has potential to affect marine phytoplankton in ways that are partly understood, but there is less knowledge about how it may alter the coupling to secondary producers. We investigated the effects of OA on phytoplankton primary production, and its trophic transfer to zooplankton in a subtropical eutrophic water (Wuyuan Bay, China) under present day (400 μatm) and projected end-of-century (1000 μatm) pCO2 levels. Net primary production was unaffected, although OA did lead to small decreases in growth rates. OA had no measurable effect on micro-/mesozooplankton grazing rates. Elevated pCO2 had no effect on phytoplankton fatty acid (FA) concentrations during exponential phase, but saturated FAs increased relative to the control during declining phase. FA profiles of mesozooplankton were unaffected. Our findings show that short-term exposure of plankton communities in eutrophic subtropical waters to projected end-of-century OA conditions has little effect on primary productivity and trophic linkage to mesozooplankton.