Microplastics are widely distributed in aquatic ecosystems along with other chemical pollutants. Therefore, it is vital to study the health-hazardous effects of MPs in combination with 4-nonylphenol (4-NP), which is a highly abundant industrial waste and a critical alkylphenol endocrine disruptor. We investigated the effects of the exposure to polyethylene microplastics (PE-MPs), 4-NP, and their combination on blood biomarkers in Cyprinus carpio juveniles. Four study groups were treated for 15 consecutive days: (1) control group, (2) 10 mg/L PE-MP group, (3) 10 mg/L PE-MPs + 200 µg/L 4-NP group, and (4) 200 µg/L 4-NP group, followed by 15 days of recovery. Biochemical analyses showed that creatine kinase, lactate dehydrogenase, glucose, liver enzymes, total protein, and A/G ratios were significantly increased after exposure to PE-MPs, 4-NP, and the combination. Hematological parameters (RBC's, Hb, Ht, neutrophil percentage, and WBC's) were significantly decreased in the three exposure groups, whereas mean corpuscular volume and lymphocyte percentages were significantly increased. The 15-day recovery period improved most hematobiochemical parameters and PE-MP accumulation indices. Taken together, we demonstrated the hazardous effects of PE-MP and 4-NP combinations on C. carpio blood parameters and highlighted their potential risk to human health.

Because nanoplastics (NPs) can transport pollutants, the absorption of surrounding pollutants into NPs and their effects are important environmental issues. This study shows a combined effect of high concentrations of NPs and copper (Cu) in the marine rotifer Brachionus plicatilis. Co-exposure decreased the growth rate, reproduction, and lifespan. The highest level of NP ingestion was detected in the co-treated group, but the Cu concentration was higher in the Cu single-exposure group. ERK activation played a key role in the downstream cell signaling pathway activated by the interaction of NPs and Cu. The increased sensitivity of B. plicatilis to Cu could be due to the impairment of MXR function caused by a high concentration of NPs, which supports our in vivo experiment results. Our results show that exposure to NPs could induce the dysfunction of several critical molecular responses, weakening resistance to Cu and thereby increasing its physiological toxicity in B. plicatilis.

Plastic pollution has been the focus of attention in recent years, with research on micro- & nano-plastics increasing exponentially. Nevertheless, several challenges associated with the small particles analysis and plastic debris assessment are still faced globally. While conducting a thorough literature review, a clear size knowledge gap between large plastics and micro- & nano-plastics is identified. This gap is evident for mesoplastics, particularly in the aims and methods to assess middle-size range plastics. Large plastic debris are likely to break into smaller fragments, and micro- & nano-plastics are continuously generated from weathered fragments due to multiple environmental stressors. Therefore, small plastic fragments (0.5–5 cm) can act as a bridge between large and micro- & nano-plastics. Here, we highlight the importance of small plastic fragment investigation to address knowledge gaps, which can be used to overcome larger management and policy challenges, while providing new insights on the plastic pollution research field.

There have been concerns about the potential health risks posed by microplastics (MP). The detection of MP in a variety of food products revealed that humans are ingesting MP. Nevertheless, there is a paucity of data about their impacts, as well as their uptake, on intestinal barrier integrity. This study examined the toxic effects of oral administration of two doses of polyethylene microplastics (PE-MP) (3.75 or 15 mg/kg/day for 5 weeks; mean particle size: 4.0–6.0 µm) on the intestinal barrier integrity in rats. Moreover, the effect of melatonin treatment with MP exposure was also assessed. The PE-MP particle uptake, histopathological changes, Alcian blue staining, Muc2 mRNA, proinflammatory cytokines (IL-1β and TNF-α), and cleaved caspase-3, as well as tight junction proteins (claudin-1, myosin light-chain kinase (MLCK), occludin, and zonula occludens-1 (ZO-1)) were assessed. Oral administration of PE-MP resulted in apparent jejunal histopathological alterations; significantly decreased mucin secretion, occludin, ZO-1, and claudin-1 expression; and significantly upregulated MLCK mRNA, IL-1β concentration, and cleaved caspase-3 expression. Melatonin reversed these altered parameters and improved the PE-MP-induced histopathological and ultrastructure changes. This study highlighted the PE-MP’s toxic effect on intestinal barrier integrity and revealed the protective effect of melatonin.

Microplastics (MPs) are an emerging threat to freshwater ecosystems with several ecotoxicological ramifications for fish. Microplastics (MPs) can adsorb heavy metals on their surfaces and increase their availability to aquatic organisms. The combined impact of lead and microplastics on fish has only been studied seldom utilizing a variety of markers. The present study aimed to evaluate the hematological, biochemical, and inflammatory signals (cytokines), as well as antioxidant enzymes in African catfish (Clarias gariepinus) exposed to lead (Pb) and MPs individually and combined for 15 days (acute toxicity experiment). The fish were split into four groups, the first of which was the control group. The second group received exposure to 1 mg/L of lead nitrate [Pb(NO₃)²]. The third group was given 100 mg/L of MPs. A solution containing 100 mg/L of MPs and 1 mg/L of lead nitrate [Pb(NO₃)²] was administered to the fourth group (the combination group). According to the findings, when MPs and Pb were combined for 15 days, the red blood cells (RBCs), thrombocytes, and lymphocytes were significantly reduced in comparison to the control fish. When compared to the control fish, the fish exposed to MPs and Pb alone or together showed a significant rise in blood interleukin-1β (IL-1β) and interleukin-6 (IL-6) cytokines. Both MPs and Pb exposure in catfish resulted in significant changes in the plasma electrolytes. The fish treated with MPs and Pb individually or in combination showed significant reduction in superoxide dismutase (SOD) and total antioxidant capacity (TAC) levels compared to the control group. The fish exposed to the combined action of MPs and Pb showed a considerable modification in all biochemical markers. The difference in the mean concentration of Pb (mg/L) between the fish exposed to Pb alone and the fish subjected to Pb and MPs combination was not statistically significant. In conclusion, according to this investigation, exposure to Pb caused an insignificant increase in Pb accumulation when MPs were present. However, co-exposure may result in anemia, cellular harm, extremely high levels of oxidative stress, and an inflammatory reaction.

Trace elements such as titanium, zirconium, thorium, and uranium, are found in black sand (BS) after weathering and corrosion. Precious metals are not the only valuable elements in black sand, rare earth elements are also found. The aquatic life in lakes and reservoirs is negatively affected by lithophilic elements such as lithium, uranium, and tin. Accordingly, intensive experiments were conducted on Nile tilapia (Oreochromis niloticus) after exposure to isolated black sand. Blood biomarkers, antioxidant balance, morpho-nuclear erythrocyte’s alterations, and histopathological signs have been investigated after fish exposure for 15 days to a 6.4 g BS/kg diet, 9.6 g BS/kg diet, and 2.4 g BS/kg diet. The blood profile, including platelets and white blood cells, was pronouncedly decreased as a result. Functions of the liver and kidneys were impaired. An increase in serum-antioxidant enzymes such as catalase activities and superoxide dismutase was recorded. Also, exposure to black sand induced cellular and nuclear abnormalities in the erythrocytes. In conclusion, the black sand isolated from the Red sea beach influenced Oreochromis niloticus’s hematology, biochemistry, and antioxidant parameters. Poikilocytosis and RBC nuclear abnormalities were also associated with exposure to black sand. The resulting erosion of rocks and rocks’ access to water forces us to consider the seriousness of climatic change on the aquatic ecosystem.

Pyrogallol promotes free radicals leading to oxidative stress and toxicity. There are however a lack of studies on oxidative stress and the antioxidant system of fish following exposure to pyrogallol. This study measured oxidative stress markers, antioxidant responses, and histological changes in catfish exposed to pyrogallol. Fish were divided into one of four experimental groups: control only, or 1, 5 or 10 mg/L pyrogallol. After 15 days, glutathione-S-transferase in the serum was decreased in fish exposed to either 5 or 10 mg/L pyrogallol relative to controls while superoxide dismutase and total antioxidant capacity were decreased significantly in fish exposed to 1, 5, or 10 mg/L pyrogallol. Conversely, catalase was increased in serum of fish exposed to 1, 5, or 10 mg/L pyrogallol compared to controls. The liver of fish treated with 1, 5, or 10 mg/L pyrogallol had significantly higher levels of oxidative stress markers (malondialdehyde, lipid peroxidation, hydroperoxide content, oxidised protein content, and DNA fragmentation %) that varied with concentration. Catfish exposed to either 1, 5, or 10 mg/L pyrogallol presented with notable histological alterations in the intestine, kidney, and muscles with prominent fibrosis, as intense deposition of collagen fibre was observed by Masson's trichrome staining. Overall, endpoints related to oxidative stress and antioxidant defence enzymes in fish may be early biomarkers of pyrogallol exposure and contamination in aquatic ecosystems. Additional studies should characterize oxidative stress indicators for their utility as biomarkers of effect.

Ochratoxin A (OTA) is a well-known mycotoxin that adversely affects different human cells. Inhalational exposure to OTA and subsequent pulmonary diseases have been previously reported, yet its potential carcinogenicity and underlying molecular mechanisms have not been fully elucidated. This study aimed to evaluate the OTA-induced cytotoxicity and the epigenetic changes underlying its potential carcinogenicity in fetal lung fibroblast (WI-38) cells. OTA cytotoxicity was assessed by MTT assay; RT-qPCR was used to determine the expression of BAX, BCL-2, TP53, and miR-155, while ELISA was used for measuring 5-methyl cytosine percentage to assess global DNA methylation in OTA-treated versus control cells. WI-38 cells demonstrated sensitivity to OTA with IC50 at 22.38 μM. Though BAX and Bcl-2 were downregulated, with low BAX/BCL-2 ratio, and TP53 was upregulated, their fold changes showed decline trend with increasing OTA concentration. A significant dose-dependent miR-155 upregulation was observed, with dynamic time-related decline. Using subtoxic OTA concentrations, a significant global DNA hypermethylation with significant dose-dependent and dynamic alterations was identified. Global DNA hypermethylation and miR-155 upregulation are epigenetic mechanisms that mediate OTA toxicity on WI-38 cells. BAX downregulation, reduced BAX/BCL-2 ratio together with miR-155 upregulation indicated either the inhibition of TP53-dependent apoptosis or a tissue specific response to OTA exposure. The aforementioned OTA-induced variations present a new molecular evidence of OTA cytotoxicity and possible carcinogenicity in lung fibroblast cells.

Due to its prevalence in aquatic environments and potential cytotoxicity, 4-nonylphenol (4-NP) has garnered considerable attention. As a medicinal plant with numerous biological activities, Nigella sativa (black seed or black cumin) seed (NSS) is widely utilized throughout the world. Consequently, this study aimed to examine the potential protective effects of NSS against 4-NP-induced hepatotoxicity in African catfish (Clarias gariepinus). To achieve this objective, 18 fish (351 ± 3 g) were randomly divided into three equal groups for 21 days. The first group serves as a control which did not receive any treatment except the basal diet. The second and third groups were exposed to 4-NP at a dose of 0.1 mg L⁻¹ of aquarium water and fed a basal diet only or supplemented with 2.5% NSS, respectively. The histological, histochemical, and ultrastructural features of the liver were subsequently evaluated as a damage biomarker of the hepatic tissue. Our results confirmed that 4-NP was a potent hepatotoxic agent, as 4-NP-intoxicated fish exhibited many lesions. Steatohepatitis, ballooning degeneration, sclerosing cholangitis, and coagulative necrosis of melanomacrophagecenters (MMCs) were observed. Hemosiderin, lipofuscin pigments, and proliferation of fibroblasts, kupffer cells, and telocytes were also demonstrated in the livers of 4-NP-intoxicated fish. In addition, decreased glycogen content and increased collagen deposition were observed in the hepatic tissue. Hepatocytes exhibited ultrastructural alterations in the chromatin, rough endoplasmic reticulum, smooth endoplasmic reticulum, mitochondria, lysosomes, and peroxisomes. Co-administration of 2.5% NSS to 4-NP-intoxicated fish significantly reduced these hepatotoxic effects. It nearly preserved the histological, histochemical, and ultrastructural integrity of hepatic tissue.