These results indicate that the abnormal sperm quality in ICR mice caused by PS-MPS exposure is closely related to the Nrf2/HO-1/NF-κB pathway.Chlamydomonas reinhardtii plays a critical role in the biogeochemical cycling of arsenic (As) and purification of water bodies contaminated with As. We investigated the effects of microplastic pollution on the ability of C. reinhardtii to accumulate As. We revealed that different sized [100 nm (S) and 5 µm (L)] polystyrene microplastics (PSMP) at different concentrations (50 and 100 mg L-1) interacted with the phospholipid structure in C. reinhardtii. Dispersion forces disrupted the structure and function of membrane proteins, reducing the accumulation and efflux of As(III) and inhibiting the As(V)-As(III)-MMA-DMA detoxification process in C. reinhardtii cells. The maximum As accumulation rates of C. BMS-935177 reinhardtii in the control groups, L50, L100, S50, and S100 treatments were 53.71, 50.95, 48.42, 43.83, and 39.11 μg g-1 h-1, respectively. Further, PSMPs and As(III) triggered “oxidative bursts” in cells, damaging cell membranes and reducing chlorophyll content and Rubisco activity. As a result, photosynthesis, respiration, and growth were inhibited. When compared with an absence of PSMP, the addition of L- (S-) sized PSMP to the As-containing solution would result in a lower (higher) impact on C. reinhardtii. Overall, this study demonstrated that microplastics significantly affect As accumulation in C. reinhardtii. Our results indicate that the critical role of this algal species in As cycling in earth’s pedo- and hydrosphere may be impeded by microplastic pollution.The occurrence and bioaccumulation of new and legacy persistent organic pollutants (POPs), organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), polychlorinated naphthalenes (PCNs), hexabromocyclododecanes (HBCDs), and Dechlorane Plus (DPs) and their related compounds (Dechloranes) in an ecosystem on King George Island, Antarctica are investigated. The new and legacy POPs were widely detected in the animal samples collected from Antarctica, which included Limpet, Antarctic cod, Amphipods, Antarctic icefish, Gentoo and Chinstrap penguins, Kelp gull, and South polar skua. The trophic magnification factors indicated that the levels of PCNs and HBCDs, as well as the legacy POPs, were magnified through the food web, whereas DPs might be diluted through the trophic levels contradicting the classification of Dechloranes as POPs. This is one of the first extensive surveys on PCNs, HBCDs, and Dechloranes, which provides unique information on the distribution and trophic biomagnification potential of the new and legacy POPs in the Antarctic region.Efficient DNA repair is essential to maintain genomic integrity. An average of 30,000 base lesions per cell are removed daily by the DNA glycosylases of the base excision repair machinery. With the advent of whole genome sequencing, many germline mutations in these DNA glycosylases have been identified and associated with various diseases, including cancer. In this graphical review, we discuss the function of the NTHL1 DNA glycosylase and how genomic mutations and altered function of this protein contributes to cancer and aging. We highlight its role in a rare tumor syndrome, NTHL1-associated polyposis (NAP), and summarize various other polymorphisms in NTHL1 that can induce early hallmarks of cancer, including genomic instability and cellular transformation.X-ray cross complementing protein 1 (XRCC1) is a DNA repair scaffold that supports base excision repair and single strand break repair, and is also a participant in other repair pathways. It also serves as an important co-transporter for several other repair proteins, including aprataxin and PNKP-like factor (APLF), and DNA Ligase 3α (LIG3). By combining highly specialized regions that help to organize specific repair functions with recruitment of additional enzymes whose contribution is dependent on the details of the damaged site, XRCC1 is able to handle an expanded range of problems that may arise as the repair progresses or in connection with other repair pathways with which it interfaces. This review discusses the interplay between these functions and considers some possible interactions that underlie its reported repair activities.Maintenance and replication of the mitochondrial genome (mtDNA) is essential to mitochondrial function and eukaryotic energy production through the electron transport chain. mtDNA is replicated by a core set of proteins Pol γ, Twinkle, and the single-stranded DNA binding protein. Fewer pathways exist for repair of mtDNA than nuclear DNA, and unrepaired damage to mtDNA may accumulate and lead to dysfunctional mitochondria. The mitochondrial genome is susceptible to damage by both endogenous and exogenous sources. Missense mutations to the nuclear genes encoding the core mtDNA replisome (POLG, POLG2, TWNK, and SSBP1) cause changes to the biochemical functions of their protein products. These protein variants can damage mtDNA and perturb oxidative phosphorylation. Ultimately, these mutations cause a diverse set of diseases that can affect virtually every system in the body. Here, we briefly review the mechanisms of mtDNA damage and the clinical consequences of disease variants of the core mtDNA replisome.In mammalian cells, the mediator protein, 53BP1, exerts distinct impacts on the repair of DNA double strand breaks (DSBs) depending on the setting, for example whether the DSBs arise at telomeres or during replication or class switch recombination. Here, we focus on two roles of 53BP1 in response to ionising radiation (IR)-induced DSBs (IR-DSBs). Canonical DNA non-homologous end-joining (c-NHEJ) is the major DSB repair pathway with homologous recombination (HR) contributing to DSB repair in S/G2 phase. ATM signalling promotes histone modifications and protein assembly in the DSB vicinity, which can be visualised as irradiation induced foci (IRIF). 53BP1 assembles at DSBs in a complex manner involving the formation of nano-domains. In G1 and G2 phase, X- or gamma-ray induced DSBs are repaired with biphasic kinetics. 70-80 % of DSBs are repaired with fast kinetics in both cell cycle phases by c-NHEJ; the remaining DSBs are repaired with slower kinetics in G2 phase via HR and in G1 by a specialised form of c-NHEJ termed Artemis and resection-dependent c-NHEJ, due to a specific requirement for the nuclease, Artemis and resection factors.