Microplastics have additive effects on cadmium accumulation and toxicity in Rice flower carp (Procypris merus).

Procypris merus, a local fish species found in Guangxi, China is often exposed to both microplastics (MPs) and Cd. However, it remains unclear how these two pollutants affect P. merus. Therefore, we investigated the effects of MPs on Cd accumulation in P. merus. To this end, P. merus was separately exposed to Cd and MPs (500 µg/L) or their combination for 14 days. We found that MPs enhanced Cd accumulation in liver and gills of P. merus. Further, both the single-contaminant (MP and Cd) and combined treatments resulted in lesions in these two tissues, with more severe damage associated with the combined treatment. Even though the effect of MP on the antioxidant defense system of P. merus was limited, the Cd-only and combined treatments considerably affected the antioxidant parameters of P. merus, with the combined treatment showing a stronger effect. GO and KEGG analyses revealed that the differentially expressed genes (DEGs; TNF-related apoptosis-inducing ligand receptor, trail-r) in the Cd-only treatment group were enriched for immune-related GO terms and cell growth and death related pathways, indicating that Cd toxicity affected immune defense in P. merus. The MP-only treatment downregulated DEGs (acyl-CoA synthetase long chain family member 1a, acsl1a) related to lipid metabolism, possibly leading to lipid accumulation in the liver. The combined treatment also upregulated DEGs (aspartate aminotransferase 1, ast 1) associated with immune-related GO terms and amino acid metabolism pathways, suggesting that it affected immune function in P. merus, thereby negatively impacting its health. Results indicated that MPs have additive effects on Cd accumulation and toxicity in rice flower carp. Consequently, MPs ingested by P. merus can promote Cd accumulation, more adverse effects on the health may occur after combined exposure, which can eventually reach humans through the food chain and pose potential risks to human health.

Humic acid addition sequence and concentration affect sulfur incorporation, electron transfer, and reactivity of sulfidated nanoscale zero-valent iron.

Nanoscale zero-valent iron (nZVI) is extensively used in field remediation and can be sulfidated in situ with sulfide or sulfate-reducing bacteria to enhance its performance. Humic acid (HA) widely exists in nature, but its influence on both the sulfidation process of nZVI and the reactivity of sulfidated nZVI (S-nZVI) has been rarely reported. Herein, we first synthesized S-nZVI by one-pot (S1-nZVI) and two-step (S2-nZVI) approaches with adding HA before (pre-added) or after (post-added) FexSy generation, respectively. Then, we evaluated their reactivity on Cr(VI) removal and analyzed the effects of HA on sulfidation regarding electron transfer resistance, sulfur incorporation, and structure characterization. Pre-added HA inhibited the Cr(VI) removal by S1-nZVI more seriously than by S2-nZVI and nZVI, and stronger inhibition was observed at higher HA concentrations. The inhibitory effect can be attributed mainly to the adsorbed HA increasing the impedance of the material and the free HA impeding the generation and deposition of FexSy. Different from the inhibition of pre-added HA at all studied HA concentrations, the Cr(VI) removal by both S1-nZVI and S2-nZVI with post-added HA was enhanced at specific HA concentrations. The reason for this phenomenon was that the dispersion and specific surface area of S-nZVI were improved, thereby offsetting the inhibition from both impedance increase and sulfur loss. This work suggests that the presence of HA can affect the sulfidation process and the property of S-nZVI, which is conducive to evaluating the performance of S-nZVI produced both by injection and in situ in the subsurface contaminant remediation.

Electroacupuncture Attenuates Immune-Inflammatory Response in Hippocampus of Rats with Vascular Dementia by Inhibiting TLR4/MyD88 Signaling Pathway.

OBJECTIVE: To investigate whether electroacupuncture (EA) alleviates cognitive impairment by suppressing the toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway, which triggers immune-inflammatory responses in the hippocampus of rats with vascular dementia (VaD). METHODS: The experiments were conducted in 3 parts and in total the Sprague-Dawley rats were randomly divided into 8 groups by a random number table, including sham, four-vessel occlusion (4-VO), 4-VO+EA, 4-VO+non-EA, sham+EA, 4-VO+lipopolysaccharide (LPS), 4-VO+LPS+EA, and 4-VO+TAK-242 groups. The VaD model was established by the 4-VO method. Seven days later, rats were treated with EA at 5 acupoints of Baihui (DV 20), Danzhong (RN 17), Geshu (BL 17), Qihai (RN 6) and Sanyinjiao (SP 6), once per day for 3 consecutive weeks. Lymphocyte subsets, lymphocyte transformation rates, and inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor α(TNF-α) were measured to assess immune function and inflammation in VaD rats. Transmission electron microscopy was used to observe the ultrastructure of nerve cells in the hippocampus. The levels of TLR4, MyD88, IL-6, and TNF-α were detected after EA treatment. TLR4/MyD88 signaling and cognitive function were also assessed after intracerebroventricular injection of TLR4 antagonist TAK-242 or TLR4 agonist LPS with or without EA. RESULTS: Compared with the 4-VO group, EA notably improved immune function of rats in the 4-VO+EA group, inhibited the protein and mRNA expressions of TLR4 and MyD88 in the hippocampus of rats, reduced the expressions of serum IL-6 and TNF-α (all P<0.05 or P<0.01), and led to neuronal repair in the hippocampus. There were no significant differences between the 4-VO+LPS+EA and 4-VO+EA groups, nor between the 4-VO+TAK-242 and 4-VO+EA groups (P>0.05). CONCLUSIONS: EA attenuated cognitive impairment associated with immune inflammation by inhibition of the TLR4/MyD88 signaling pathway. Thus, EA may be a promising alternative therapy for the treatment of VaD.