Concurrent water- and foodborne exposure to microplastics leads to differential microplastic ingestion and neurotoxic effects in zebrafish.

Organisms constantly ingest microplastics directly from the environment or indirectly via trophic transfer due to the pervasiveness of microplastic pollution. However, most previous studies have only focused on waterborne exposure at the individual level, while few studies have investigated the contribution of trophic transfer to the exposure in organisms. We comprehensively evaluated the differences in microplastic ingestion and toxic effects in zebrafish exposed to microplastics via two concurrent routes (waterborne and foodborne). The polyethylene microplastics (40-47 µm, 0.1-10 mg/L) concentration used here was set in a range closed to the environmentally relevant microplastic concentrations, especially considering the extreme high concentration scenarios in wastewater. The concentration of microplastics resulting from foodborne exposure (0.01±0.01 µg/mg; 0.1±0.1 particles/mg) was significantly lower than that through waterborne exposure (0.06±0.02 µg/mg; 0.8±0.3 particles/mg), suggesting the ingestion of microplastics in their tissues occurs mainly through direct environmental uptake rather than food chain transfer (though the initial microplastic concentration was 1000 folds lower). However, more sublethal impacts, including the significant abnormal hyperactive swimming behaviour (107±5% induction; p< 0.05), were observed in the foodborne group than waterborne group. Additionally, ingenuity pathway analysis predicted both exposure routes caused obvious nervous system interference but through opposite modes of action. This was further verified by the alteration of neurotransmitter biomarkers that neurotoxicity mechanisms were completely different for the two exposure routes. The neurotoxic effects of microplastics are non-negligible and can exert together through both water- and foodborne exposure routes, which deserves further attention.

Rethinking the relevance of microplastics as vector for anthropogenic contaminants: Adsorption of toxicants to microplastics during exposure in a highly polluted stream - Analytical quantification and assessment of toxic effects in zebrafish (Danio rerio).

Given the increasing amounts of plastic debris entering marine and freshwater ecosystems, there is a growing demand for environmentally relevant exposure scenarios to improve the risk assessment of microplastic particles (MPs) in aquatic environments. So far, data on adverse effects in aquatic organisms induced by naturally exposed MPs are scarce and controversially discussed. As a consequence, we investigated the potential role of MPs regarding the sorption and transfer of environmental contaminants under natural conditions. For this end, a mixture of four common polymer types (polyethylene, polypropylene, polystyrene, polyvinyl chloride) was exposed to natural surface water in a polluted stream for three weeks. Samples of water, MP mixture, sediment, and suspended matter were target-screened for the presence of pollutants using GC/LC-MS, resulting in up to 94 different compounds. Possible adverse effects were investigated using several biomarkers in early developmental stages of zebrafish (Danio rerio). Exposure to natural stream water samples significantly inhibited acetylcholinesterase activity, altered CYP450 induction and modified behavioral patterns of zebrafish. In contrast, effects by samples of both non-exposed MPs and exposed MPs in zebrafish were less prominent than effects by water samples. In fact, the analytical target screening documented only few compounds sorbed to natural particles and MPs. Regarding acute toxic effects, no clear differentiation between different MPs and natural particles could be made, suggesting that - upon exposure in natural water bodies - MPs seem to approximate the sorption behavior of natural particles, presumably to a large extent due to biofilm formation. Thus, if compared to natural inorganic particles, MPs most likely do not transfer elevated amounts of environmental pollutants to biota and, therefore, do not pose a specific additional threat to aquatic organisms.

Fluoride-Induced Expression of Neuroinflammatory Markers and Neurophysiological Regulation in the Brain of Wistar Rat Model.

Excess fluoride intake has been linked with various pathological conditions. The objective of the present study was to understand the role of fluoride in neurotoxic, neuroinflammatory, and neurodegenerative changes in the brain tissue of Wistar rats. Wistar rats were fed with water containing 20-100 ppm (ppm) sodium fluoride (NaF). An array of neurotransmitters (acetylcholine, dopamine, epinephrine, norepinephrine, serotonin, histamine, and glutamate) expression levels were estimated with respect to different fluoride concentrations. Additionally, its effect on the expression levels of specific neuroinflammatory markers (iNOS, COX-2, TNF-α, PKC, VEGF, and HSP-70) in brain tissues of Wister rats was assessed. An increase in NaF concentration resulted in increased fluoride deposition in the brain which in turn caused increase levels of epinephrine, histamine, serotonin, and glutamate and decreased levels of norepinephrine, acetylcholine, and dopamine in a dose-dependent manner. Tissue fluoride levels of the hippocampus, neocortex, cerebellum, spinal cord, and sciatic nerve increased significantly in fluoride fed rats. Transmission electron microscopy in the experimental animals revealed axon deterioration, myelin sheath degeneration, and dark cells with scanty cytoplasm in the spinal cord and sciatic nerve. Additionally, vacuolated swollen mitochondria were observed in the neocortex, hippocampus, and cerebellum. Results suggest excess fluoride intake modulates a set of biological marker and promote neuroinflammatory and neurodegenerative condition in Wister rats. Therefore, we conclude that the accumulation of NaF alters the neurological function which leads to neurodegenerative disorders.

Massive extrusion of calcium hydroxide paste containing barium sulphate during endodontic treatment.

A 31-year-old woman was referred for the evaluation of persistent lower lip numbness following endodontic treatment of tooth #36. Imaging examinations showed a large amount of radiopaque/hyperdense material spread in an angiographic distribution in the left mandibular body region. Laboratory analyses of tooth #36 and adjacent periapical tissue, surgically extracted in an external Service due to acute pain following endodontic treatment, identified chronic inflammatory reaction and birefringent crystalloid foreign bodies rich in barium and sulphur, leading to the diagnosis of alveolar nerve injury due to accidental extrusion of intracanal dressing material composed of calcium hydroxide [Ca(OH)2 ] paste incorporated with barium sulphate. Clinicians should be aware that Ca(OH)2 when in contact with periapical tissues may lead to persistent toxicities, such as necrosis, pain and paraesthesia. Therefore, injectable Ca(OH)2 systems should be used with caution because they can cause paste extrusion and damage to the lower alveolar nerve.

Accidental injury of the inferior alveolar nerve due to the extrusion of calcium hydroxide in endodontic treatment: a case report.

During clinical endodontic treatment, we often find radiopaque filling material beyond the root apex. Accidental extrusion of calcium hydroxide could cause the injury of inferior alveolar nerve, such as paresthesia or continuous inflammatory response. This case report presents the extrusion of calcium hydroxide and treatment procedures including surgical intervention. A 48 yr old female patient experienced Calcipex II extrusion in to the inferior alveolar canal on left mandibular area during endodontic treatment. After completion of endodontic treatment on left mandibular first molar, surgical intervention was planned under general anesthesia. After cortical bone osteotomy and debridement, neuroma resection and neurorrhaphy was performed, and prognosis was observed. But no improvement in sensory nerve was seen following surgical intervention after 20 mon. A clinician should be aware of extrusion of intracanal medicaments and the possibility of damage on inferior alveolar canal. Injectable type of calcium hydroxide should be applied with care for preventing nerve injury. The alternative delivery method such as lentulo spiral was suggested on the posterior mandibular molar.