Cadmium (Cd) accumulation in Solanum nigrum L. is known to occur mainly in cell walls and vesicles. However, limited research has been conducted on the toxic effects of Cd specifically targeting mitochondria in S. nigrum leaves. This study aims to delineate the impact of Cd accumulation on mitochondrial structure and function in S. nigrum leaves, thereby providing a theoretical foundation for enhancing its application in phytoremediation of Cd-polluted soils. The results showed that the Cd content in mitochondria would gradually reach saturation with the increase of Cd treatment concentration. However, the accumulation of Cd led to osmotic pressure imbalance and morphological changes within mitochondria, which in turn caused a series of impairments in mitochondrial function. Cd severely damaged the energy metabolism function of mitochondria, especially under 200 mu M CdCl2 stress, the mitochondrial ATP content decreased by 90.65 % and the activity of H+-ATPase decreased by 80.65 %. Furthermore, reactive oxygen species (ROS) in mitochondria accumulated mainly in the form of H2O2. Compared with the non-Cd control group, the H2O2 content in the Cd-treated groups (50, 100, and 200 mu M CdCl2) increased by 61.62 %, 186.69 %, and 405.81 %, respectively. The inhibition of cellular respiration by Cd and the sharp increase in ROS exacerbated the oxidative damage in mitochondria. Interestingly, the activities of mitochondrial peroxidase (POD) and dehydroascorbate reductase (DHAR) exhibit remarkable tolerance under Cd stress. Based on these results, we believe that Cd can cause dysfunction and oxidative damage to the mitochondria of S. nigrum leaves.

Alzheimer's disease (AD) is a complex neurodegenerative disorder that is classically defined by the extracellular deposition of senile plaques rich in amyloid-beta (A beta) protein and the intracellular accumulation of neurofibrillary tangles (NFTs) that are rich in aberrantly modified tau protein. In addition to aggregative and proteostatic abnormalities, neurons affected by AD also frequently possess dysfunctional mitochondria and disrupted mitochondrial maintenance, such as the inability to eliminate damaged mitochondria via mitophagy. Decades have been spent interrogating the etiopathogenesis of AD, and contributions from model organism research have aided in developing a more fundamental understanding of molecular dysfunction caused by A beta and toxic tau aggregates. The soil nematode C. elegans is a genetic model organism that has been widely used for interrogating neurodegenerative mechanisms including AD. In this review, we discuss the advantages and limitations of the many C. elegans AD models, with a special focus and discussion on how mitochondrial quality control pathways (namely mitophagy) may contribute to AD development. We also summarize evidence on how targeting mitophagy has been therapeutically beneficial in AD. Lastly, we delineate possible mechanisms that can work alone or in concert to ultimately lead to mitophagy impairment in neurons and may contribute to AD etiopathology.

The escalating utilization of carbon dots (CDs) in agriculture raises ecological concerns. However, their combined toxicity with arsenic remains poorly understood. Herein, we investigated the combined mitochondrial genotoxicity of CDs and arsenate at environmentally relevant concentrations across successive earthworm generations. Iron-doped CDs (CDs(-Fe)) strongly bound to arsenate and arsenite, while nitrogen-doped CDs (CDs(-N)) exhibited weaker binding. Both CDs enhanced arsenate bioaccumulation without affecting its biotransformation, with most arsenate being reduced to arsenite. CDs(-Fe) generated significantly more reactive oxygen species than did CDs-N, causing stronger mitochondrial DNA (mtDNA) damage. Arsenate further exacerbated the oxidative mtDNA damage induced by CDs(-N), as evidenced by increased reactive oxygen species, elevated 8-oxo-7,8-dihydro-2 '-deoxyguanosine (8-OHdG) levels, and a higher correlation between 8-OHdG and mtDNA damage. This was due to arsenic inhibiting the antioxidant enzyme catalase. This exacerbation was negligible with CDs(-Fe) because their strong binding with arsenic prevented catalase inhibition. Maternal mitochondrial DNA damage was inherited by filial earthworms, which experienced significant weight loss in coexposure groups coupled with mtDNA toxicity. This study reveals the synergistic genotoxicity of CDs and arsenate, suggesting that CDs could disrupt the arsenic biogeochemical cycle, increase arsenate risk to terrestrial animals, and influence ecosystem stability and health through multigenerational impacts.

The microplastics and organic additives formed in routine use of plastic takeaway food containers may pose significant health risks. Thus, we collected plastic containers made of polystyrene, polypropylene, polyethylene terephthalate, polylactic acid and simulated two thermal usages, including hot water (I) and microwave treatments (M). Nile Red fluorescence staining was developed to improve accurate counting of microplastics with the aid of TEM and DLS analysis. The quantity of MPs released from thermal treatments was determined ranging from 285.7 thousand items/cm(2) to 681.5 thousand items/cm(2) in containers loaded with hot water with the following order: IPS>IPP>IPET>IPLA, while microwave treatment showed lower values ranging from 171.9 thousand items/cm(2) to 301.6 thousand items/cm(2). In vitro toxicity test using human intestinal epithelial Caco-2 cells indicated decrease of cell viability in raw leachate, resuspended MPs and supernatants, which might further lead to cell membrane rupture, ROS production, and decreased mitochondrial membrane potential. Moreover, the leachate inhibited the expression of key genes in the electron transport chain (ETC) process, disrupted energy metabolism. For the first time, we isolate the actually released microplastics and organic substances for in vitro toxicity testing, and demonstrate their potential impacts to human intestine.

As an environmental pollution metal, copper (Cu) exposure -induced toxicity is closely related to mitochondrial damage. Mitochondrial-derived vesicles (MDVs) plays an essential role in mitochondrial quality control and cellular metabolism. However, the mechanism by which MDVs are involved in cellular metabolism under Cu exposure remains unclear. Here, the MDV-carrying protein MIGA2 was identified as a crucial molecule involved in the Cu -induced autophagosomes-lysosomes fusion. Furthermore, Cu exposure significantly promoted MDVs secretion, accompanied by a markedly increased MIGA2 expression in MDVs, as well as accelerated the autophagosomes-lysosomes fusion. However, small RNA interference of SNX9 (the MDVs secretion inductor) and MIGA2 blocked autophagic flux induced by Cu, leading to failure of autophagosomes degradation. Coimmunoprecipitation assay further demonstrated that ATG14 was a regulation target protein of MIGA2. Overexpression and knockdown of ATG14 significantly affected the autophagosomes-lysosomes fusion induced by Cu. Meanwhile, knockdown of ATG14 dramatically reversed the effect of MIGA2-overexpression in promoting autophagosomes-lysosomes fusion, while overexpression of ATG14 shows the opposite effect. These results demonstrated that MDVs-carrying MIGA2 protein promoted autophagosomes-lysosomes fusion induced by Cu. This study demonstrated that MDVs is involved in regulating organelles -to -organelles communication, providing a new insight into the toxicity mechanism of Cu exposure on hepatocytes.

Iron is a common and essential element for maintaining life in bacteria, plants and animals and is found in soil, fresh waters and marine waters; however, over exposure is toxic to organisms. Iron is used in electron transport complexes within mitochondria as well as a co-factor in many essential proteins. It is also established that iron accumulation in the central nervous system in mammals is associated with various neurological disorders. Ample studies have investigated the long-term effects of iron overload in the nervous system. However, its acute effects in nervous tissue and additional organ systems warrant further studies. This study investigates the effects of iron overload on development, behavior, survival, cardiac function, and glutamatergic synaptic transmission in the Drosophila melanogaster. Additionally, physiological responses in crayfish were examined following Fe3+ exposure. Fe3+ reduced neuronal excitability in proprioceptive neurons in a crayfish model. Thus, Fe3+ may block stretch activated channels (SACs) as well as voltage-gated Na+ channels. Exposure also rapidly reduces synaptic transmission but does not block ionotropic glutamatergic receptors, suggesting a blockage of pre-synaptic voltage-gated Ca2+ channels in both crustacean and Drosophila models. The effects are partly reversible with acute exposure, indicating the cells are not rapidly damaged. This study is relevant in demonstrating the effects of Fe3+ on various physiological functions in different organisms in order to further understand the acute and long-term consequences of overload.

Microplastics have emerged as significant and concerning pollutants within soil ecosystems. Among the soil biota, entomopathogenic nematodes (EPNs) are lethal parasites of arthropods, and are considered among the most effective biological agents against pests. Infective juveniles (IJs) of EPNs, as they navigate the soil matrix scavenging for arthropod hosts to infect, they could potentially encounter microplastics. Howver, the impact of microplastics on EPNs has not been fully elucidated yet. We addressed this gap by subjecting Steinernema feltiae EPNs to polystyrene microplastics (PS-MPs) with various sizes, concentrations, and exposure durations. After confirming PS-MP ingestion by S. feltiae using fluorescent dyes, we found that the PS-MPs reduced the survival, reproduction, and pathogenicity of the tested EPNs, with effects intensifying for smaller PS-MPs (0.1-1 mu m) at higher concentrations (105 mu g/L). Furthermore, exposure to PS-MPs triggered oxidative stress in S. feltiae, leading to increased reactive oxygen species levels, compromised mitochondrial membrane potential, and increased antioxidative enzyme activity. Furthermore, transcriptome analyses revealed PS-MP-induced suppression of mitochondrial function and oxidative phosphorylation pathways. In conclusion, we show that ingestion of PSMPs by EPNs can compromise their fitness, due to multple toxicity effects. Our results bear far-reaching consequences, as the presence of microplastics in soil ecosystems could undermine the ecological role of EPNs in regulating pest populations.

The increasing popularity of seed treatment applications in agriculture may leave unintended hazards to soil biota, such as earthworms. The objective of this study was to explore mitochondrial DNA toxicity resulting from sublethal exposures to systemic pesticides, including four neonicotinoid insecticides (neonics), as well as coexposure to difenoconazole (DIF), a triazole fungicide, in earthworms (Eisenia fetida) in vivo. Earthworms were exposed under dose regimes resembling label recommendation and levels left in soil post seed treatment application for 30 days in an earthworm breeding facility. Mitochondrial DNA copy numbers (mtDNAcn) in earthworms were determined by using the 2(-Delta Ct) algorithm. Earthworms' body weights were recorded before and after the exposure period. We found a highly significant increase of mtDNAcn in earthworms across all exposure groups (ANOVA, p < 0.001), either under a single neonic or combined with DIF exposure. Coupled with mtDNA toxicity, earthworms in the treatment groups gained significantly less weight than control earthworms (ANOVA, p < 0.001). We concluded that systemic pesticides, both neonics and DIF, posed mtDNA toxicity as measured by mtDNAcn, in earthworms.

Intensive poultry production may result in substantial emissions of pollutants into the environment, including pharmaceuticals and other chemicals used in poultry farming. The objective of this study was to verify the presence of ciprofloxacin, enrofloxacin, carbamazepine, metoclopramide, trimethoprim, diflufenican, flufenacet, and p,p '-DDE in soil and water in the immediate vicinity of a poultry manure heap. The influence of soil contaminants on the growth and selected physiological parameters of seed peas and common duckweed (as indicator plants) was tested. It has been proven that the cultivation of pea plants on soil coming from the close proximity of a heap of manure results in a deterioration of both morphological parameters (root length, shoot length) and physiological parameters (chlorophyll absorption, aminolevulinic acid dehydrogenase (ALAD) activity, aminolevulinic acid (ALA) content, lipid peroxidation, mitochondrial damage or production of HSP70 proteins). Similarly, water extracts from cultivated soils had a significant effect on duckweed, and it was found that contaminant leachates are indeed detectable in soil, groundwater, and deep water. Special attention should, therefore, be paid to the location, methods of storage, and use of poultry fertilizer.