The aim of the present study was to evaluate Vitamin C (VC) as a potent natural antioxidant to mitigate the genotoxic effects of Arsenic trioxide and sodium fluoride in Swiss albino mice in vivo. The study was divided into eight groups consisting of control treated with normal saline (Group I), Group II, III, IV, V, VI, VII and the VC group with only Vitamin C (500 mg/kgbw). Arsenic trioxide (4 mg/kgbw) and Sodium fluoride (8 mg/kgbw) were administered singly, as well as in combination to swiss albino mice, with and without VC. In this study, the genotoxic effect of arsenic (As) and fluoride (F) in mice using comet, chromosomal aberration and lipid peroxidation assay was investigated. The results revealed that VC efficiently ameliorates the genotoxic effect of As and F by increasing the frequency of chromosomal aberrations and primary DNA damage along with increased malondialdehyde (MDA) level. In conclusion, VC mitigates the genotoxic effects of the two well-known water contaminants (As and F) effectively and efficiently at the given concentration in vivo.

Both noise and shift work generate oxidative stress, independently; however, in some work places workers are exposed to both at the same time, where their combined effect might increase the oxidative damage. This research is based on the question whether noise and shift work have a synergistic effect on oxidative stress or not. It tries to investigate the effects of these two factors simultaneously, at the biggest cement factory of Iran. For so doing, it enrols 88 male workers, equally in four groups, with one group serving as the control (i.e., Group 1 with 8 hours of fixed shift, exposed to less than 85 dB sound level) and three groups as the cases (Group 2 with 12 hours of rotational shifts, exposed to less than 85 dB sound level; Group 3 with 8 hours of fixed shift, exposed to more than 85 dB sound level; and Group 4 with 12 hours of rotational shifts, exposed to more than 85 dB sound level). Stress oxidative is evaluated by Malondialdehyde (MDA) and Superoxide dismutase (SOD).  Finally, the results show that SOD levels (p<0.001) are significantly decreased in Group 4 and Group 3, compared to the control. Also, MDA levels are significantly increased in Group 4 (in which, the workers are exposed to noise and shift work simultaneously) compared to the control (p < 0.001). The current study shows that co-exposure to noise and shift work has a combined effect (a synergistic role) in MDA. Thereore, more attention should be paid to shift workers, who are exposure to noise simultaneously.

Bibliometric network analysis has revealed that the widespread distribution of microplastics (MPs) has detrimental effects on marine organisms; however, the combined effects of MPs and climate change (e.g., warming) is not well understood. In this study, Prorocentrum donghaiense, a typical red tide species in the East China Sea, was exposed to different MP concentrations (0, 1, 5, and 10 mg L⁻¹) and temperatures (16, 22, and 28 °C) for 7 days to investigate the combined effects of MPs and simulated ocean warming by measuring different physiological parameters, such as cell growth, pigment contents (chlorophyll a and carotenoid), relative electron transfer rate (rETR), reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), and adenosine triphosphate (ATP). The results demonstrated that MPs significantly decreased cell growth, pigment contents, and rETRₘₐₓ, but increased the MDA, ROS, and SOD levels for all MP treatments at low temperature (16 °C). However, high temperatures (22 and 28 °C) increased the pigment contents and rETRₘₐₓ, but decreased the SOD and MDA levels. Positive and negative effects of high temperatures (22 or 28 °C) were observed at low (1 and 5 mg L⁻¹) and high MP (10 mg L⁻¹) concentrations, respectively, indicating the antagonistic and synergistic effects of combined warming and MP pollution. These results imply that the effects of MPs on microalgae will likely not be substantial in future warming scenarios if MP concentrations are controlled at a certain level. These findings expand the current knowledge of microalgae in response to increasing MP pollution in future warming scenarios.

Nowadays, the ubiquitous distribution and increasing abundance of P⁺ᴵᴵᴵ in waterbodies have caused serious concerns regarding its bioavailability and potential toxicity. However, our knowledge on these issues is relatively limited. We addressed previously unknown effects of P⁺ᴵᴵᴵ on three dominate algae species i.e. Microcystic aeruginosa (M. aeruginosa), Chlorella pyrenoidesa (C. pyrenoidesa) and Cyclotella. sp in eutrophic waterbodies in China. Remarkable declines in biomass, specific growth rate and Chl-a of algae cells treated with 0.01–0.7 mg/L P⁺ᴵᴵᴵ as sole or an alternative P source were observed, indicating P⁺ᴵᴵᴵ had an inhibitory effect on the algal growth. Besides, the intracellular enzyme activities e.g superoxide dismutase (SOD) and malondialdehyde (MDA) were significantly increased with P⁺ᴵᴵᴵ stress. M. aeruginosa and Cyclotella. sp cells seemed to be more sensitive to P⁺ᴵᴵᴵ toxicity than C. pyrenoidesa since cell membrane suffered more serious stress and destruction. These findings combined, it confirmed P⁺ᴵᴵᴵ could not be utilized as bioavailable P, but had certain toxicity to the tested algae. It indicated that the increased P⁺ᴵᴵᴵ abundance in eutrophic waterbodies would accelerate the algal cell death, which could have a positive effect against algal blooms. Our results provide new insights into assessing the ecological risks of P⁺ᴵᴵᴵ in aquatic environments.

A broad-spectrum fungicide, dichlofluanid is widely used in antifouling paints and agricultural pesticides. In this study, the acute and chronic effects of sublethal concentrations, namely, no observable effect concentration (NOEC) and 50% lethal concentration (LC₅₀) of dichlofluanid (1/10 NOEC, NOEC, 1/10 LC₅₀, and LC₅₀) were evaluated on the marine mysid, Neomysis awatschensis. Acute toxicity test (96 h) showed higher sensitivity to dichlofluanid in juvenile mysids (LC₅₀ 3.1 μg L⁻¹) than adults (LC₅₀ 24.5 μg L⁻¹), with lower survival rate and reduction in food consumption. Exposure with dichlofluanid considerably induced oxidative imbalance, as NOEC (0.006 μg L⁻¹ for juveniles and 0.074 μg L⁻¹ for adults) and 1/10 LC₅₀ values increased intracellular concentrations of malondialdehyde and glutathione, and the enzymatic activities of catalase and superoxide dismutase, whereas exposure to LC₅₀ value decreased the values of oxidative parameters. Enzymatic activity of acetylcholinesterase decreased considerably when exposed to LC₅₀ value. In the case of chronic effects, exposure to NOEC for 4 weeks markedly decreased the juvenile survival rate, while adults showed tolerance. Multigenerational monitoring in response to NOEC showed a significant growth retardation with an increase in intermolt duration as well as a decrease in the number of newborn mysids from females of the third generation. Consistent exposure to environmentally relevant sublethal concentrations of dichlofluanid would be detrimental to mysid individuals and the survival of the mysid population.

To examine the potential role of acetate in conferring cadmium (Cd) stress tolerance in lentil (Lens culinaris), several phenotypical and physio-biochemical properties have been examined in Cd-stressed lentil seedlings following acetate applications. Acetate treatment inhibited the translocation of Cd from roots to shoots, which resulted in a minimal reduction in photosynthetic pigment contents. Additionally, acetate-treated lentil showed higher shoot (1.1 and 11.72%) and root (4.98 and 30.64%) dry weights compared with acetate-non-treated plants under low-Cd and high-Cd concentrations, respectively. Concurrently, acetate treatments increase osmoprotection under low-Cd stress through proline accumulation (24.69%), as well as enhancement of antioxidant defense by increasing ascorbic acid content (239.13%) and catalase activity (148.51%) under high-Cd stress. Acetate-induced antioxidant defense resulted in a significant diminution in hydrogen peroxide, malondialdehyde and electrolyte leakage in Cd-stressed lentil seedlings. Our results indicated that acetate application mitigated oxidative stress-induced damage by modulating antioxidant defense and osmoprotection, and reducing root-to-shoot Cd transport. These findings indicate an important contribution of acetate in mitigating the Cd toxicity during growth and development of lentil seedlings, and suggest that the exogenous applications of acetate could be an economical and new avenue for controlling heavy metal-caused damage in lentil, and potentially in many other crops.

This study focused on the impacts of aged aquaculture microplastics (MPs) on oysters (Crassostrea gigas). Adult oysters were exposed for two months to a cocktail of MPs representative of the contamination of the Pertuis Charentais area (Bay of Biscay, France) and issuing from oyster framing material. The MPs mixture included 28% of polyethylene, 40% of polypropylene and 32% of PVC (polyvinyl chloride). During the exposure, tissues were sampled for various analyzes (MP quantification, toxicity biomarkers). Although no effect on the growth of adult oysters was noted, the mortality rate of bivalves exposed to MPs (0.1 and 10 mg. L⁻¹ MP) increased significantly (respectively 13.3 and 23.3% of mortalities cumulative). On the one hand, the responses of biomarkers revealed impacts on oxidative stress, lipid peroxidation and environmental stress. At 56 days of exposure, significant increases were noted for Glutathione S-Transferase (GST, 10 mg. L⁻¹ MP), Malondialdehyde (MDA, 10 mg. L⁻¹ MP) and Laccase (LAC, 0.1 and 10 mg. L⁻¹ MP). No variations were observed for Superoxyde Dismutase (SOD). Besides, ingestion of MPs in oyster tissues and the presence in biodeposits was highlighted. In addition, in vitro fertilisations were performed to characterize MPs effects on the offspring. Swimming behavior, development and growth of D-larvae were analysed at 24-, 48- and 72-h after fertilisation. D-larvae, from exposed parents, demonstrated reduced locomotor activity. Developmental abnormalities and arrest as well as growth retardation were also noted. This study highlighted direct and intergenerational effects of MPs from aged plastic materials on Pacific oysters.

Humans benefit from nuclear technologies but consequently experience nuclear disasters or side effects of iatrogenic radiation. Hematopoietic system injury first arises upon radiation exposure. As an intricate new layer of genetic control, the posttranscriptional m⁶A modification of RNA has recently come under investigation and has been demonstrated to play pivotal roles in multiple physiological and pathological processes. However, how the m⁶A methylome functions in the hematopoietic system after irradiation remains ambiguous. Here, we uncovered the time-varying epitranscriptome-wide m⁶A methylome and transcriptome alterations in γ-ray-exposed mouse bone marrow. 4 Gy γ-irradiation rapidly (5 min and 2 h) and severely impaired the mouse hematopoietic system, including spleen and thymus weight, blood components, tissue inflammation and malondialdehyde (MDA) levels. The m⁶A content and expression of m⁶A related enzymes were altered. Gamma-irradiation triggered dynamic and reversible m⁶A modification profiles and altered mRNA expression, where both m⁶A fold-enrichment and mRNA expression most followed the (5 min_up/2 h_down) pattern. The CDS enrichment region preferentially upregulated m⁶A peaks at 5 min. Moreover, the main GO and KEGG pathways were closely related to metabolism and the classical radiation response. Finally, m⁶A modifications correlated with transcriptional regulation of genes in multiple aspects. Blocking the expression of m⁶A demethylases FTO and ALKBH5 mitigated radiation hematopoietic toxicity. Together, our findings present the comprehensive landscape of mRNA m⁶A methylation in the mouse hematopoietic system in response to γ-irradiation, shedding light on the significance of m⁶A modifications in mammalian radiobiology. Regulation of the epitranscriptome may be exploited as a strategy against radiation damage.

Hydrogen peroxide (H₂O₂), as a common disinfectant, has been extensively used in aquaculture. The toxicity of high ambient H₂O₂ for gills and liver of fish has received attention from many researchers. However, whether H₂O₂ exposure induced brain injury and neurotoxicity has not been reported in fish. Therefore, this study aimed to explore the potential mechanism of H₂O₂ toxicity in brain of common carp via transcriptome analysis and biochemical parameter detection. The fish were exposed to 0 (control) and 1 mM of H₂O₂ for 1 h per day lasting 14 days. The results showed that H₂O₂ exposure caused oxidative damage in brain evidenced by decreased glutathione (GSH), total antioxidant capacity (T-AOC) and nicotinamide adenine dinucleotide (NAD⁺) levels, and increased formation of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Meanwhile, H₂O₂ exposure reduced 5-hydroxytryptamine (5-HT) level, and down-regulated tryptophan hydroxylase 1 (tph1a), tph2, 5-hydroxytryptamine receptor 1A-beta (htr1ab) and htr2b expression in brain. Transcriptome analysis showed that H₂O₂ exposure up-regulated 604 genes and down-regulated 1209 genes in brain. Go enrichment displayed that the differently expressed genes (DEGs) were enriched mainly in cellular process, single-organism process, metabolic process, and biological regulation in the biological process category. Further, KEGG enrichment indicated that H₂O₂ exposure led to dysregulation of neurotransmitter signals including depression of glutamatergic synapse, GABAergic synapse and endocannabinoid signaling. Also, we found the alteration of three key pathways including calcium, cAMP and HIF-1 in brain after H₂O₂ exposure. In conclusion, our data indicated that H₂O₂ exposure induced oxidative damage and neurotoxicity, possibly related to dysregulation of neurotransmitters and calcium, cAMP and HIF-1 signaling pathways, which may adversely affect learning, memory and social responses of common carp. This study provided novel insight into biological effects and underlying mechanism of H₂O₂ toxicity in aquatic animal, and contributed to proper application of H₂O₂ in aquaculture.

Nuclear factor-erythroid 2-related factor-2 (Nrf2) is an important modulator of cellular responses against Cd in mammalian cells. However, whether such modulation is conserved in Marsupenaeus japonicas remains unknown.In our study, the shrimps were injected with dsRNA targeting Nrf2 at 4 μg g⁻¹ body weight (b.w.) or sulforaphane (SFN) at 5 μg g⁻¹ b.w., and then were exposed to 40 mg L⁻¹ CdCl₂ for 48 h. After Nrf2 knockdown, the Cd content increased, but decreased in the SFN group. This suggested that Nrf2 could promote Cd excretion. A terminal deoxynulceotidyl transferase nick-end-labeling (TUNEL) assay revealed that the Nrf2 knockdown increased the number of apoptotic cells in M. japonicas, while SFN decreased the number of apoptotic cells. After Nrf2 knockdown, the total antioxidant capacity (T-AOC), superoxide dismutase (Sod) activity, and related gene expression decreased significantly, while the malondialdehyde (MDA) content increased remarkably. By contrast, SFN injection alleviated the oxidative stress, as evidenced by increased T-AOC, Sod activity, sod mRNA expression and a reduced MDA content. Similarly, detoxification related enzyme activities (ethoxyresorufin O-deethylase and glutathione-S-transferase (GST)) and their corresponding gene expressions (cyp3a (cytochrome P450 family 3 subfamily A) and gst) were suppressed in the ds-Nrf2 injection group, while they were elevated in the SFN group. In addition, ds-Nrf2 activated mitochondrial apoptotic pathway, as evidenced the mRNA and protein levels of caspase-3, Bcl2 associated X protein (Bax), and p53, while SFN treatment suppressed them. These results displayed that in M. japonicus Cd-induced cellular oxidative damage probably acts via the Nrf2 pathway.