Diel Fluctuation Superimposed on Steady High <i>p</i>CO₂ Generates the Most Serious Cadmium Toxicity to Marine Copepods

Coastal systems experience diel fluctuation of pCO2 and cadmium (Cd) pollution; nevertheless, the effect of fluctuating pCO2 on Cd biotoxicity is poorly known. In this study, we initially performed the isotopically enriched organism bioassay to label Tigriopus japonicus with 113Cd (5 μg/L) to determine the Cd accumulation rate constant (kaccu) under ambient (400 μatm) and steadily (1000 μatm) and fluctuatingly elevated (1000 ± 600 μatm) pCO2 conditions for 48 h. Next, T. japonicus was interactively subjected to the above pCO2 exposures at Cd (control, 5, and 500 μg/L) treatments for 7 d. Biochemical and physiological responses for copepods were analyzed. The results showed that steadily increased pCO2 facilitated Cd bioaccumulation compared to ambient pCO2, and it was more under fluctuating acidification conditions. Despite compensatory reactions (e.g., increased energy production), Cd ultimately induced oxidative damage and apoptosis. Meanwhile, combined treatment exhibited higher toxicity (e.g., increased apoptosis) relative to Cd exposure, and even more if fluctuating acidification was considered. Intriguingly, fluctuating acidification inhibited Cd exclusion in Cd-treated copepods compared to steady acidification, linking to higher Cd kaccu and bioaccumulation. Collectively, CO2-driven acidification could aggravate Cd toxicity, providing a mechanistic understanding of the interaction between seawater acidification and Cd pollution in marine copepods

Kaplan-Meier analysis of cancer-specific survival.

<p>KIF26B protein levels showed prognostic role in overall survival <b>(A)</b> and disease-free survival <b>(B)</b>.</p

Univariate analysis of various variables.

*<p>Statistical significant.</p

KIF26B mRNA and protein expression in breast cancer.

<p><b>A,</b> KIF26B mRNA was upregulation in 27 of 30 breast cancer cases. The relative KIF26B mRNA expression was indicated by histogram (Tumor, primary breast cancer tissues; Normal, the paired adjacent normal breast tissues). <b>B,</b> The KIF26B mRNA levels was significantly upregulation in breast cancer as determined by matched paired Students' <i>t</i> test. <b>C,</b> KIF26B protein expression was upregulation in 26 of 30 breast cancer cases by western blot. β-actin was used as the loading control.</p

Immunohistochemical analysis of KIF26B in breast cancer.

<p>Normal breast contains rare KIF26B-positive cells <b>(A)</b>, whereas breast cancer tissues show weak <b>(B)</b>, moderate <b>(C)</b>, and strong <b>(D)</b> staining of KIF26B. Numerical scores: A = 0, B = 2, C = 6, D = 12.</p

Relationship between clinicopathologic factors and KIF26B expression.

*<p>Statistical significant.</p