Colonization characteristics and surface effects of microplastic biofilms: Implications for environmental behavior of typical pollutants.

This paper summarizes the colonization dynamics of biofilms on microplastics (MPs) surfaces in aquatic environments, encompassing bacterial characteristics, environmental factors affecting biofilm formation, and matrix types and characteristics. The interaction between biofilm and MPs was also discussed. Through summarizing recent literatures, it was found that MPs surfaces offer numerous benefits to microorganisms, including nutrient enrichment and enhanced resistance to environmental stress. Biofilm colonization changes the surface physical and chemical properties as well as the transport behavior of MPs. At the same time, biofilms also play an important role in the fragmentation and degradation of MPs. In addition, we also investigated the coexistence level, adsorption mechanism, enrichment, and transformation of MPs by environmental pollutants mediated by biofilms. Moreover, an interesting aspect about the colonization of biofilms was discussed. Biofilm colonization not only had a great effect on the accumulation of heavy metals by MPs, but also affects the interaction between particles and environmental pollutants, thereby changing their toxic effects and increasing the difficulty of MPs treatment. Consequently, further attention and research are warranted to delve into the internal mechanisms, environmental risks, and the control of the coexistence of MPs and biofilms.

Strategy and mechanisms of sulfamethoxazole removal from aqueous systems by single and combined Shewanella oneidensis MR-1 and nanoscale zero-valent iron-enriched biochar.

Sulfamethoxazole (SMX, a sulfonamide antibiotic) is ubiquitously present in various aqueous systems, which can accelerate the spread of antibiotic resistance genes, induce genetic mutations, and even disrupt the ecological equilibrium. Considering the potential eco-environmental risk of SMX, this study explored an effective technology using Shewanella oneidensis MR-1 (MR-1) and nanoscale zero-valent iron-enriched biochar (nZVI-HBC) to remove SMX from aqueous systems with different pollution levels (1-30 mg·L-1). SMX removal by nZVI-HBC and nZVI-HBC + MR-1 (55-100 %) under optimal conditions (iron/HBC ratio of 1:5, 4 g·L-1 nZVI-HBC, and 10 % v/v MR-1) was more effective than its removal by MR-1 and biochar (HBC) (8-35 %). This was due to the catalytic degradation of SMX in the nZVI-HBC and nZVI-HBC + MR-1 reaction systems because of accelerated electron transfer during oxidation of nZVI and reduction of Fe(III) to Fe(II). When SMX concentration was lower than 10 mg·L-1, nZVI-HBC + MR-1 effectively removed SMX (removal rate of approximately 100 %) when compared to nZVI-HBC (removal rate of 56-79 %). In addition to oxidation degradation of SMX by nZVI in the nZVI-HBC + MR-1 reaction system, MR-1-driven dissimilatory iron reduction accelerated electron transfer to SMX, thereby enhancing reductive degradation of SMX. However, a considerable decline in SMX removal from the nZVI-HBC + MR-1 system (42 %) was observed when SMX concentrations ranged 15-30 mg·L-1, which was due to the toxicity of accumulated degradation products of SMX. A high interaction probability between SMX and nZVI-HBC promoted the catalytic degradation of SMX in the nZVI-HBC reaction system. The results of this study provide promising strategies and insights for enhancing antibiotic removal from aqueous systems with different pollution levels.

Monosialoganglioside protects against bupivacaine-induced neurotoxicity caused by endoplasmic reticulum stress in rats.

BACKGROUND: Local anesthetics in spinal anesthesia have neurotoxic effects, resulting in severe neurological complications. Intrathecal monosialoganglioside (GM1) administration has a therapeutic effect on bupivacaine-induced neurotoxicity. The aim of this study was to determine the underlying mechanisms of bupivacaine-induced neurotoxicity and the potential neuroprotective role of GM1. MATERIALS AND METHODS: A rat spinal cord neurotoxicity model was established by injecting bupivacaine (5%, 0.12 µL/g) intrathecally. The protective effect of GM1 (30 mg/kg) was evaluated by pretreating the animals with it prior to the bupivacaine regimen. The neurological and locomotor functions were assessed using standard tests. The histomorphological changes, neuron degeneration and apoptosis, and endoplasmic reticulum stress (ERS) relevant markers were analyzed using immunofluorescence, quantitative real-time PCR, and Western blotting. RESULTS: Bupivacaine resulted in significant neurotoxicity in the form of aberrant neurolocomoter functions and spinal cord histomorphology and neuronal apoptosis. Furthermore, the ERS specific markers were significantly upregulated during bupivacaine-induced neurotoxicity. These neurotoxic effects were ameliorated by GM1. CONCLUSION: Pretreatment with GM1 protects against bupivacaine-induced neurotoxicity via the inhibition of the GRP78/PERK/eIF2α/ATF4-mediated ERS.

Therapeutic effects of intrathecal versus intravenous monosialoganglioside against bupivacaine-induced spinal neurotoxicity in rats.

BACKGROUND: Bupivacaine causes neuronal and axonal degeneration, leading to cauda equina syndrome or permanent nerve damage. Our previous studies have shown that intrathecal or intravenous gangliosides monosialogangliosides (GM-1s) have therapeutic effects against bupivacaine-induced neurotoxicity, but we do not know what are the differences between the two methods. METHODS AND RESULTS: Bupivacaine-induced neurotoxicity was induced in rats by three times injection of 5% bupivacaine (0.24µl/g) to the L3 spinal cord. We observed by H&E staining that bupivacaine caused obvious neuronal injuries in the spinal cord, such as edema, vacuolation of myelin sheaths, and neuronal degeneration. Electron microscopy revealed similar pathohistological changes. Neural functions, evaluated by tail-flicking test and locomotor scaling, were also impaired. Treatment with GM-1s (30mg/kg) repaired the neural lesions and gradually improved the neural functions. By days 14 and 28 post GM-1s, the pathohistological changes in the posterior root and posterior column had significantly recovered but not completely. Compared with intravenous routes, intrathecal application of GM-1s demonstrated faster and greater efficacies in regeneration of neural damages and in improvement of neural dysfunctions. Caspase-3, a marker of cellular apoptosis, was shown by immunohistochemistry to be suppressed in protein transcription by GM-1s application and intrathecal GM-1s had potentiated a greater reduction in caspase-3 protein than intravenous GM-1s. CONCLUSIONS: Treatment with GM-1s in intrathecal routes more effectively reverses bupivacaine-induced neural injuries and improves the neural dysfunctions than intravenous routes. This may be partly attributed to that GM-1 inhibits the expression of cellular apoptosis factor caspase-3 protein.