Screening the Efficacy and Safety of Molluscicides from Three Leaf Extracts of Chimonanthus against the Invasive Apple Snail, Pomacea canaliculata.

Pomacea canaliculata, the invasive snail, is a host of the parasitic nematode Angiostrongylus cantonensis, which has adverse effects on the agriculture system and human health. This work evaluated the molluscicidal activity of petroleum ether extracts (PEEs) from three species of Chimonanthus against the snail P. canaliculate. Pcp (PEE of C. praecox) showed the most effective molluscicide activity. Sixty-one compounds were identified by GC-MS and the main components were terpenoids and fatty acids. The half-lethal concentration (LC50) of Pcp at 24 h (0.27 mg/mL) and 48 h (0.19 mg/mL) was used to evaluate the biochemical alterations in snail tissue. These sublethal concentrations caused the levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activity to increase, while acetylcholinesterase (AChE) activity decreased. Also, under LC50 treatment, several histological changes were observed in the hepatopancreas and foot of the snail compared with the control group. Moreover, the toxic test in rice demonstrated that Pcp has low toxicity. These results suggest that Pcp could be developed as an effective molluscicide for P. canaliculata control.

A multidisciplinary study on Clinostomum infections in Nile tilapia: micro-morphology, oxidative stress, immunology, and histopathology.

Yellow grub disease, caused by Clinostomum metacercaria, is an endemic zoonotic infection in freshwater fish, responsible for Halzoun syndrome transmitted through the consumption of raw infected fish. This study aimed to conduct a multidisciplinary investigation integrating detailed morphology, oxidative stress, immunology, and histopathology alteration to advance our understanding of Clinostomum infection. In this annual study, 400 Nile tilapia (Oreochromis niloticus) were collected from the Nile River at Al Bahr Al Aazam, Giza Governorate to assess Clinostomum infection prevalence. Of the examined fish, 160 individuals (40.0%) harboured larval Clinostomum infections. Clinostomum metacercariae were observed in various anatomical locations, with 135 fish (33.8%) in buccal cavities, 21 fish (5.25%) in gill chambers, and 4 fish (1.0%) on the skin. Infection intensity ranged from 2 to 12 cysts per fish, averaging 5 cysts, notably with skin infections characterized by a single cyst in each fish. Macroscopic encysted metacercariae were collected from buccal cavities, gills, and skin. Micro-morphology revealed distinct features in C. complanatum, including an elliptical oral sucker with collar-like rings and large sensory papilla-like structures, contrasting with the absence of these features in C. phalacrocoracis. Oxidative stress, assessed through malondialdehyde (MDA) and nitric oxide levels, revealed an elevation in MDA to 35.13 ± 6 nmol/g and nitric oxide to 25.80 ± 3.12 µmol/g in infected fish. In infected fish, MHC-I gene expression increased approximately 13-fold, MHC-II peaked at 19-fold, and IL-1ß significantly upregulated by 17-fold, compared to control levels. Histopathology detailed associated lesions, such as cyst encapsulation and eosinophilic infiltration. Clinstomiasis and its impacts on fish hosts offer crucial insights to control this emerging fish-borne zoonotic disease, threatening wildlife, aquaculture, and human health.

Biomarkers of oral subacute toxicity of deltamethrin in exposed male Albino rats.

Deltamethrin is one of the most effective pyrethroid compounds, widely employed in veterinary medicine, public health, and farming. Deltamethrin-triggered oxidative stress largely causes serious harm to an organism. Acute toxicity of this compound was extensively investigated, while less information is available on its oral sub-acute effects. This study assessed, in the male Albino rats, the effects of oral gavage of either 0.874 mg/kg (0.01 LD50) or 8.740 mg/kg (0.10 LD50) of deltamethrin for successive 14 days to investigate its effects on biomarkers and to detect the tissue injury in rats following subacute deltamethrin treatment. It was found that levels of glutathione peroxidase, superoxide dismutase, and catalase in the brain, kidney, and liver, alkaline phosphatase (ALP), and uric acid in serum, hematocrit, mean corpuscular volume (MCV), white blood cells (WBC)s, eosinophils, and basophils were significantly reduced compared with untreated rats. However, when rats were treated with deltamethrin for successive 14 days, alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activities in serum and the levels of thiobarbituric acid reactive substances (TBARs) in brain, kidney, and liver, red blood cell distribution width (RDW-CV), total protein, monocytes, and basophils and the ratios of neutrophils to lymphocytes, an aggregated marker of systemic inflammation and systemic immune inflammation indexes, significantly increased compared with the control group. Histologic lesions were observed in the liver, kidney, brain, testis, and epidemies in rats exposed to subacute deltamethrin for 14 days, and most tissues of rats treated with 0.10 LD50 of deltamethrin were more affected than those treated with 0.01 LD50. These findings strongly suggest that subacute exposure to deltamethrin caused significant systemic toxicity through oxidative stress resulting in biochemical and histological changes in the studied tissues. These findings highlight the potential harmful effects of deltamethrin and emphasize the importance of understanding the subacute effects of this compound, particularly in the context of veterinary medicine, public health, and farming.

New insights into the oxidative damage and antioxidant defense mechanism in Manila clams (Ruditapes philippinarum) exposed to 8:2 polyfluoroalkyl phosphate diester stress.

8:2 perfluoroalkyl phosphate diester (8:2 diPAP) is the main precursor of perfluoroalkyl carboxylic acids, and it has been detected in a wide range of environments. In this study, conventional biochemical and histopathological analyses and transcriptome methods were used to investigate the accumulation and oxidative stress of 8:2 diPAP in Manila clams (Ruditapes philippinarum) as well as the clam's defense mechanisms for the first time. The hepatopancreas was the main target organ for 8:2 diPAP accumulation; the concentration reached 484.0 ±â€¯15.5 ng/g after 7 days of exposure to 10 µg/L of 8:2 diPAP, which was 2-100 times higher than that found in other organs. 8:2 diPAP accumulation resulted in significant lipid peroxidation, and the change in malondialdehyde content was highly correlated with 8:2 diPAP accumulation (r > 0.8). The antioxidant enzymes catalase and peroxidase were significantly activated at 7 days of exposure. Although the levels subsequently returned to normal, this restoration was unable to prevent damage. Histopathological analysis showed that 8:2 diPAP exposure resulted in inflammatory damage to the hepatopancreas, which failed to resolve during the recovery period. Transcriptomic analyses showed that the expression of differentially expressed genes had different degrees of positive/negative correlation with antioxidant indicators, and they were significantly enriched in cell death regulatory pathways such as autophagy, apoptosis, and necrosis. The core factor expression results indicated that 8:2 diPAP exposure induced activation of the organismal autophagy factor followed by a shift towards apoptosis. In addition, pathways related to amino acid metabolism and energy metabolism were involved in determining the cell fate of Manila clams. Overall, these results indicated that 8:2 diPAP induced peroxidation of membrane lipids, disturbed physiological processes, and ultimately initiated programmed cell death in Manila clams. The findings of this study provide new insights into the mechanism of toxicity of 8:2 diPAP exposure in marine bivalves.

Cellular, histological, and behavioral pathological alterations associated with the mouse model of photothrombotic ischemic stroke.

BACKGROUND: Photothrombotic (PT) stroke model is a reliable method to induce ischemic stroke in the target site using the excitation of photosensitive agents such as Rose Bengal (RB) dye after light illumination. Here, we performed a PT-induced brain ischemic model using a green laser and photosensitive agent RB and confirmed its efficiency through cellular, histological, and neurobehavioral approaches. METHODS: Mice were randomly allocated into RB; Laser irradiation; and RB + Laser irradiation groups. Mice were exposed to a green laser at a wavelength of 532 nm and intensity of 150 mW in a mouse model after injection of RB under stereotactic surgery. The pattern of Hemorrhagic and ischemic changes were evaluated throughout the study. The volume of the lesion site was calculated using unbiased stereological methods. For investigation of neurogenesis, we performed double - (BrdU/NeuN) immunofluorescence (IF) staining on day 28 following the last- BrdU injection. To assess the effect and quality of ischemic stroke on neurological behavior, the Modified neurological severity score (mNSS) test was done on days 1, 7, 14, and 28 days after stroke induction. RESULTS: Laser irradiation plus RB induced hemorrhagic tissue and pale ischemic changes over the 5 days. In the next few days, microscopic staining revealed neural tissue degeneration, demarcated necrotic site, and neuronal injury. BrdU staining showed a significant number of proliferating cells in the periphery of the lesion site in the Laser irradiation plus RB group compared to the group (p < 0.05) while the percent of NeuN+ cells per BrdU- positive cells was reduced. Also, prominent astrogliosis was observed in the periphery of irradiated sites on day 28. Neurological deficits were detected in mice from Laser irradiation plus the RB group. No histological or functional deficits were detected in RB and Laser irradiation groups. CONCLUSIONS: Taken together, our study showed cellular and histologic pathological changes which are associated with the PT induction model. Our findings indicated that the undesirable microenvironment and inflammatory conditions could affect neurogenesis concomitantly with functional deficits. Moreover, this research showed that this model is a focal, reproducible, noninvasive and accessible stroke model with a distinctive demarcation similar to human stroke conditions.

Thyroid endocrine disruption and neurotoxicity of gestodene in adult female mosquitofish (Gambusia affinis).

The frequent detection of progestins in various aquatic environments and their potential endocrine disruptive effects in fish have attracted increasing attention worldwide. However, data on their effects on thyroid function and neurotoxicity in fish are limited, and the underlying mechanisms remain unclear. Here, the effects of gestodene (GES, a common progestin) on the thyroid endocrine and nervous systems of mosquitofish (Gambusia affinis) were studied. Adult female fish were exposed to GES at environmentally relevant concentrations (4.4-378.7 ng/L) for 60 days. The results showed that exposure to 378.7 ng/L GES caused a significant decrease in fish growth compared with the control and a marked reduction in the total distance traveled (50.6%) and swimming velocity (40.1-61.9%). The triiodothyronine (T3) levels were significantly increased by GES in a dose-dependent manner, whereas those of tetraiodothyronine (T4) were significantly decreased only at the G500 concentration. The acetylcholinesterase (AChE) activity was decreased significantly in the 4.42 ng/L GES treatments, but increased significantly at 378.67 ng/L. In the brain, a strong increase in the transcriptional levels of bdnf, trh, and dio2 was observed in fish after the 378.7 ng/L treatment. In addition, chronic exposure to GES caused colloid depletion with a concentration-dependent manner in the thyroid, and angiectasis, congestion, and vacuolar necrosis in the brain. These findings provide a better understanding of the effects of GES and associated underlying mechanisms in G. affinis.

Risk Assessment and Hazardous Effects of Metal Contamination in O. niloticus and S. galilaeus from Four Islands of the River Nile.

The Nile River islands are recognized as the most productive lands in Egypt. Although, these islands are vulnerable to several natural and man-made crises. The present study was aimed to evaluate the consequences of different anthropogenic activities on the heavy metals load and histological alterations in O. niloticus and S. galilaeus collected from four different Nile River islands along the Great Cairo sector (Egypt), and the possible health risks for human consumers. Metals were accumulated in both fish muscles in the following order: Fe > Zn > Cu > Mn > Pb. S. galilaeus was recorded higher metal pollution index than O. niloticus, while El-Warrak Island was documented the highest MPI and hazard quotient among all sampling sites. All sampled tissues were recorded histopathological lesions in both fish. The present study may be considered as an early alert for habitual consumers, particularly at high consumption rates of some fish species.

Dietary Parsley Seed Mitigates Methomyl-Induced Impaired Growth Performance, Hemato-Immune Suppression, Oxidative Stress, Hepato-Renal Damage, and Pseudomonas aeruginosa Susceptibility in Oreochromis niloticus.

The present experiment investigated the potential protective role of parsley (Petroselinum crispum) seed meal (PSM) in alleviating methomyl (MET)-adverse impacts on growth, whole-body composition, hematological indicators, hepatorenal function, immune response, oxidative status, and disease resistance to Pseudomonas aeruginosa. For this purpose, 225 healthy Nile tilapia (Oreochromis niloticus) were allotted into five groups (45 fish/group in triplicate). One group was reared in clean water and fed a non-supplemented basal diet, while the other groups were exposed to 20.39 µg L-1 MET and fed a non-fortified basal diet or basal diets supplemented with 0.5, 1.0, or 2.0% of PSM for 60 days. The obtained data revealed significantly lower weight gain, feed intake, and specific growth rate, but higher feed conversion ratio and decreases in crude protein, lipid, and ash contents in the MET-exposed fish. Anemia, leukopenia, lymphocytopenia, and esonipenia were also obvious. Furthermore, MET-exposed fish had significantly higher serum levels of hepatic enzymes and renal damage products. Nevertheless, there was a significant depletion of enzymatic and non-enzymatic antioxidants and increased malondialdehyde, myeloperoxidase, and tumor necrosis factor-α levels in MET-exposed fish. The MET exposure significantly depressed lysozyme activity, nitric oxide, complement3, acetylcholinesterase activity, total proteins, globulin, and albumin levels in O. niloticus serum. Furthermore, pathological alterations in the liver and kidney were noted. The relative percentage of survival rate in MET-exposed fish was dramatically reduced on day 14 post-challenge with P. aeruginosa. The inclusion of PSM, on the other hand, greatly alleviated most of the MET-related negative effects. Taken together, the dietary intervention with PSM has a promising role in alleviating MET-deleterious impacts, rendering parsley seeds a viable aqua feed additive for O. niloticus.

Antioxidant enzyme activity and pathophysiological responses in the freshwater walking catfish, Clarias batrachus Linn under sub-chronic and chronic exposures to the neonicotinoid, Thiamethoxam®.

The hydrophilic nature and resultant persistence of neonicotinoids in aquatic systems increase the exposure duration for non-target organisms. The sublethal toxicity of the neonicotinoid Thiamethoxam® spanning sub-chronic and chronic durations was investigated in Clarias batrachus, a non-target freshwater fish species. 96 h LC50 value of Thiamethoxam® on Clarias batrachus was 138.60 mg L-1. Pre-determined exposure concentrations of Thiamethoxam® (6.93 and 13.86 mg L-1) were used and effects were assessed at days 15, 30, and 45 exposure intervals. Biomarker effects were evaluated using antioxidant enzyme responses (CAT, SOD) neurotransmission (acetylcholinesterase activity), haematological and serum biochemistry changes (including haemoglobin content, total erythrocyte count, and serum albumin total leukocyte count, total serum protein, serum globulin, triglyceride, cholesterol, high-density lipoprotein, very low-density lipoprotein, low-density lipoprotein, phospholipid, and total serum glucose), histopathological alterations (gill and liver). Thiamethoxam®-exposed fish showed a marked reduction in haemoglobin content, total erythrocyte count, and serum albumin levels compared to control fish. Similarly, gill and liver antioxidant enzyme activity (CAT, SOD) and neurotransmission (acetylcholinesterase) also showed altered responses between sub-chronic exposure on day-15 and chronic responses on day-45. Histopathological observations in gill tissue revealed alterations ranging from vacuolation, hypertrophy, disruption of primary lamellar architecture, haemorrhage, the fusion of secondary lamella, and sloughing of outer epithelia. For liver tissue of exposed fish histopathological observations included increased sinusoidal spaces (ISS), necrosis of hepatocytes (NOH), nuclear degeneration (ND), disruption of architecture (DOA), macrophage infiltration of the central vein, vacuolation (V), hypertrophied hepatocytes, and haemorrhages. The gradients of toxic responses across exposure concentrations and depictions of impaired fish health with increasing thiamethoxam® exposure duration portend lowered physiological capacity for survival in the wild.

Mercuric chloride-induced oxidative stress, genotoxicity, haematological changes and histopathological alterations in fish Channa punctatus (Bloch, 1793).

The present study was undertaken to investigate the adverse effects of mercuric chloride (HgCl2 ) overload in the fish Channa punctatus. Two sublethal test concentrations of HgCl2 (1/20th and 1/10th of 96 h LC50 i.e., 0.03 mg l-1 (low concentration) and 0.07 mg l-1 (high concentration), respectively, were used for exposure. Blood, liver and kidney tissues of the control and exposed specimens were sampled at intervals of 15, 30, and 45 days to assess alterations in oxidative stress, genotoxicity haematological parameters and histopathology. Significant changes in Hb%, RBC count, WBC count, antioxidant enzyme activity, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione reductase (GR), were recorded. Micronuclei (MN) induction, nuclear abnormalities (NAs) and histopathological alterations were also observed in the exposed fish. Significant (P < 0.05) increase in the activities of SOD, CAT, GSH and GR was observed. After 45 days, a decrease in the level of GSH and GR was noticed which suggests an undermined anti-oxidative defence system in the fish exposed to HgCl2 . Histological examination of the liver and kidney showed serious tissue injury and histological alterations. Significant increases in MN and NA frequencies reveal the DNA damage in erythrocytes of fish, and haematological changes show the toxicological potential of HgCl2 . The observed changes in the antioxidant defence system, genotoxicity and haematological and histological changes in the present study provide the most extensive insight into HgCl2 stress in C. punctatus.

Low concentrations of ciprofloxacin alone and in combination with paracetamol induce oxidative stress, upregulation of apoptotic-related genes, histological alterations in the liver, and genotoxicity in Danio rerio.

Nowadays, there are countless articles about the harmful effects of paracetamol (PCM) in non-target organisms. Nonetheless, information regarding the toxicity of ciprofloxacin (CPX) and the CPX-PCM mixture is still limited. Herein, we aimed to evaluate the hepatotoxic and genotoxic effects that ciprofloxacin alone and in combination with paracetamol may induce in Danio rerio adults. For this purpose, we exposed several D. rerio adults to three environmentally relevant concentrations of PCM (0.125, 0.250, and 0.500 µg/L), CPX (0.250, 0.500, and 1 µg/L), and their mixture (0.125 + 0.250, 0.250 + 0.500, and 0.500 + 1 µg/L) for 96 h. The blood samples showed CPX alone and in combination with PCM damaged the liver function of fish by increasing the serum levels of liver enzymes alanine aminotransferase and alkaline phosphatase. Moreover, our histopathological study demonstrated liver of fish suffered several tissue alterations, such as congestion, hyperemia, infiltration, sinusoidal dilatation, macrovascular fatty degeneration, and pyknotic nuclei after exposure to CPX alone and in combination with PCM. Concerning oxidative stress biomarkers and the expression of genes, we demonstrated that CPX and its mixture, with PCM, increased the levels of antioxidant enzymes and oxidative damage biomarkers and altered the expression of Nrf1, Nrf2, BAX, and CASP3, 6, 8, and 9 in the liver of fish. Last but not least, we demonstrated CPX alone and with PCM induced DNA damage via comet assay and increased the frequency of micronuclei in a concentration-dependent manner in fish. Overall, our results let us point out CPX, even at low concentrations, induces hepatotoxic effects in fish and that its combination with PCM has a negative synergic effect in the liver of this organism.

Behavioral, physiological and biochemical responses and differential gene expression in Mytilus galloprovincialis exposed to 17 alpha-ethinylestradiol and sodium lauryl sulfate.

Mixture of contaminants often determine biological responses of marine species, making difficult the interpretation of toxicological data. The pharmaceutical 17 alpha-ethinylestradiol (EE2) and the surfactant Sodium Lauryl Sulfate (SLS) commonly co-occur in the marine environment. This study evaluated the effects of EE2 (125.0 ng/L) and SLS (4 mg/L), acting individually and combined, in the mussel Mytilus galloprovincialis. Contaminated mussels closed their valves for longer periods than control ones, especially in the presence of both contaminants, with longer closure periods immediately after spiking compared to values obtained one day after spiking. Nevertheless, males and females increased their metabolism when in the presence of both contaminants (males) and SLS (females), and independently on the treatment males and females were able to activate their antioxidant and biotransformation defences. Although enhancing defences mussels still presented cellular damage and loss of redox balance, especially noticed in the presence of EE2 for males and SLS for females. Histopathological damage was found at mussel's gills in single and mixture exposure, and qPCR analysis revealed a clear estrogen receptor expression with no additive effect due to combined stressors. The results obtained highlight the harmful capacity of both contaminants but further research on this matter is needed, namely considering different climate change scenarios.

Evaluation of Nephrotoxicity in Oreochromis niloticus After Exposure to Aluminum Oxide Nanoparticles: Exposure and Recovery Study.

Nephrotoxic impacts of Al2O3 nanoparticles (NPs) were studied in Oreochromis niloticus after seven days of exposure and fifteen days of recovery periods. Fish were classified as group I (dechlorinated water); group II (2 mg/L Al2O3NPs); group III (4 mg/L Al2O3NPs); group IV (8 mg/L Al2O3NPs). Blood creatinine and uric acid levels showed marked increases in groups III and IV. A dose-dependent disturbance in renal antioxidant components was recorded as indicated by elevated catalase, superoxide dismutase, thiobarbituric acid reactive substances levels, and decreased glutathione reduced concentration. Renal histopathology was recorded with the highest % of appearance in group IV. A reduction in renal Al content, kidney function biomarkers (excepting group IV), and enhanced antioxidant status were observed after applying a recovery strategy. Several structural damages were identified following the recovery period, but the alteration frequencies indicated regressive histopathological changes. The Al2O3NPs-induced nephrotoxicity can be reduced after applying a suitable recovery period.

The Danubian cryptic invader Theodoxus fluviatilis (Gastropoda: Neritidae) in the River Rhine: a potential indicator for metal pollution?

Metal pollution poses a major threat to aquatic systems especially in anthropogenic influenced areas, in as much as metals are persistent in the environment. The freshwater snail Theodoxus fluviatilis has often been used as an indicator species for the ecological status in river monitoring. In the River Rhine, the native Northern-European form of T. fluviatilis is nowadays extinct, whilst the Danubian form is spreading along the river. The aim of our study was to investigate if the cryptic invader is affected by metal exposure present in the River Rhine and to discuss its potential as an indicator for metal pollution. Several environmental abiotic (14 water environmental variables plus five common metal concentrations in water and biofilm) and biotic parameters (biofilm mass) were measured across 23 sites along the River Rhine. Five population and six histopathological parameters were evaluated on snails collected at all 23 sites. Aqueous chromium concentration was positively correlated to the damage of male reproductive organs of T. fluviatilis, and higher ammonium concentration was correlated to a decrease in snail size and an increase in the proportion of juveniles. None of the analysed snail parameters was negatively correlated to concentrations of other metals measured, like copper and zinc. Therefore, based on the parameters evaluated, our results indicate that the Danubian form of T. fluviatilis is only restrictedly suitable as an indicator for metal pollution in the River Rhine system. Further field and laboratory investigations including other stressors are necessary to evaluate the indicator potential of the cryptic invader holistically.

How temperature rise will influence the toxic impacts of 17 α-ethinylestradiol in Mytilus galloprovincialis?

Pharmaceutical drugs are Contaminants of Emerging Concern (CECs) and are continuously discharged into the environment. As a result of human and veterinary use, these substances are reaching aquatic coastal systems, with limited information regarding the toxic effects of these compounds towards inhabiting organisms. Among CECs are pharmaceuticals like 17 α-ethinylestradiol (EE2), which is a synthetic hormone with high estrogenic potency. EE2 has been increasingly found in different aquatic systems but few studies addressed its potential toxicity to marine wildlife, in particular to bivalves. Therefore, the aim of the present study was to evaluate the influence of temperature (17 °C-control and 21 °C) on the potential effects of EE2 on the mussel Mytilus galloprovincialis. For this purpose, mussels were exposed to different concentrations of EE2 (5.0; 25.0; 125.0 and 625 ng/L), resembling low to highly polluted sites. Mussels exposed to each concentration were maintained under two temperatures, 17 and 21 °C, which represent actual and predicted warming conditions, respectively. After 28 days, oxidative stress status, metabolism related parameters, neurotoxicity and histopathological alterations were measured. The results obtained clearly showed an interactive effect of increased temperature and EE2, with limited antioxidant and biotransformation capacity when both stressors were acting together, leading to higher cellular damage. The combination of both stressors also enhanced mussels' metabolic capacity and neurotoxic effects. Nevertheless, loss of redox balance was confirmed by the strong decrease of the ratio between reduce glutathione (GSH) and oxidized glutathione (GSSG) in contaminated mussels, regardless the temperature. Histopathological indexes in contaminated mussels were significantly different from the control group, indicating impacts in gills and digestive glands of mussels due to EE2, with higher values observed at 21 °C. Overall, this study demonstrates that of EE2 represents a threat to mussels and predicted warming conditions will enhance the impacts, which in a near future might result in impairments at the population and community levels.

Potential role of dietary chitosan nanoparticles against immunosuppression, inflammation, oxidative stress, and histopathological alterations induced by pendimethalin toxicity in Nile tilapia.

A 21-days feeding screening period was conducted to highlight the protective efficacy of dietary chitosan nanoparticles (CSNPs) on pendimethalin (PD)-induced toxicity in Nile tilapia (Oreochromis niloticus). Hematology, non-specific immune response, the antioxidative enzymes [superoxide dismutase (SOD) and catalase (CAT), glutathione reduced (GSH), and glutathione peroxidase (GPx)] in the liver and anterior kidney, changes of pro-inflammatory cytokine genes [interleukins-8 (IL-8), interleukins-1ß (IL-1ß), and tumor necrosis-α (TNF-α)] in the anterior kidney and histopathological alterations were assessed. Fish (50 ± 7.5 g) were randomly assigned into four groups (Three replicates), the first group served as the negative control and fed on the control diet only, and the second group served as the positive control and fed on the control diet supplemented with CSNPs (1 g kg-1 diet). The two other groups were exposed to 1/10 96-h LC50 PD (0.5 mg L-1) in rearing water and simultaneously fed the control diet alone or supplemented with CSNPs (1 g kg-1 diet), respectively. Fish were fed on the experimental diets twice a day for 21 days. The results revealed that PD exposure caused a significant decline in the survival rate of the Nile tilapia, as well as in most of the hematological indices, respiratory burst activity, phagocytic activity, total immunoglobulin levels, lysozyme, and bactericidal activity. Additionally, PD toxicity markedly suppressed most of the antioxidative enzymatic activities in both tissues together with upregulation of immune genes (IL-8 and TNF-α); however, IL-1ß expression remained unaffected. The histopathological results revealed marked pathological changes in spleen, liver and intestine with a notable decrease of intestinal goblet cells in PD-exposed groups. Conversely, CSNPs exerted protective effects through improving the above mentioned parameters. Thus, CSNPs supplementation exhibited defensive effects against PD toxicity in Nile tilapia that might provide an insight into the promising role of CSNPs as a potential immunomodulatory feed additive for tilapia in aquaculture.

Impact of copper oxide nanoparticles on the cerebral cortex of adult male albino rats and the potential protective role of crocin.

The use of copper oxide nanoparticles (CUONPs) on a large-scale application is a reason for many health problems and morbidities involving most body tissues, particularly those of the nervous system. Crocin is the chemical ingredient primarily responsible for the color of saffron. It has different pharmacological effects, such as antioxidant, anticancer, and memory-improving activities. This study was conducted to elaborate the effects of CUONP exposureon the cerebellar cortical tissues of rats and explore the potential protecting role of crocin through biochemical, light microscopic, and ultrastructural examinations. Twenty four adult male albino rats were randomly divided into four equal groups: Group I (negative control); Group II (crocin-treated group; 30mg/kg body weight (BW) intraperitoneal (IP) crocin daily); Group III (CUONP-treatedgroup; 0.5-mg/kg BW IP CUONP daily); and Group IV (CUONP/crocin-treated group). After 14 days of the experiment, venous blood samples were collected to determine red blood cell (RBC), white blood cell (WBC), and hemoglobin (Hb) levels. Besides, serum malondialdehyde (MDA), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were measured. Cerebellar tissue samples were examined under light and electron microscopy along with a histomorphological analysis. CUONPs induced oxidative/antioxidative imbalance as evidenced by a significant increase in serum MDA levels and decreased GPx and TAC activities. CUONPs caused a significant decrease in RBC and Hb levels and an increase in WBC count. Histopathological alterations in the cerebellar cortex were observed. The administration of crocin showed some protection against the toxic effects of CUONPs. Crocin is suggested to have a mitigating role on oxidative stress and structure alterations in the cerebellar tissues induced by CUONPs.

Nannochloropsis oculata feed additive alleviates mercuric chloride-induced toxicity in Nile tilapia (Oreochromis niloticus).

Using microalgae to alleviate the adverse effects of aquaculture pollutants, including metals, has recently gained much attention. In this context, bioaccumulation, hematological indices, oxidative and antioxidant responses, and histopathological alterations were investigated in Nile tilapia (Oreochromis niloticus) fed with either a control diet or diets containing Nannochloropsis oculata (N. oculata) after exposure to mercuric chloride in order to evaluate the role of this microalgae in protecting against mercury-induced toxicity. Fish exposed to HgCl2 at a dose of » LC50 (0.3 mg/L) (Hg group) for 7-21 days exhibited a significant increase in total mercury concentration with a bioaccumulation pattern of liver>gills>muscle, and a significant decrease in all blood indices except mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), monocyte counts, and neutrophil counts. Malondialdehyde (MDA) levels were significantly increased in the Hg group at all time points relative to the control. Glutathione peroxidase (GPx) activity was significantly increased at days 14 and 21, while catalase (CAT) and GPx activities increased and decreased, respectively, at day 7 compared to the control. Additionally, lysozyme activity and immunoglobulin M (IgM) were significantly decreased in the Hg-exposed group. Severe histopathological alterations were evident in the liver, kidneys, and gills. However, supplementation with N. oculata at a low (5%, 50 g/kg feed) or high (10%, 100 g/kg feed) dose stabilized all parameters and reduced the severity of the histopathological alterations with the high N. oculata diet showing more prominent effects. These results suggest that feeding N. oculata protects Nile tilapia against mercuric chloride-induced toxicity.

Effects of temperature on caffeine and carbon nanotubes co-exposure in Ruditapes philippinarum.

In the marine environment, organisms are exposed to a high and increasing number of different contaminants that can interact among them. In addition, abiotic factors can change the dynamics between contaminants and organisms, thus increasing or even decreasing the toxic effect of a particular compound. In this study, the effects of caffeine (CAF) and functionalized multi-walled carbon nanotubes (f-MWCNTs) induced in the clam Ruditapes philippinarum were evaluated, acting alone and in combination (MIX), under two temperature levels (18 and 21 °C). To assess the impact of such compounds, their interaction and the possible influence of temperature, biochemical and histopathological markers were investigated. The effects of f-MWCNTs and caffeine appear to be clearly negative at the control temperature, with lower protein content in contaminated clams and a significant decrease in their metabolism when both pollutants were acting in combination. Also, at control temperature, clams exposed to pollutants showed increased antioxidant capacity, especially when caffeine was acting alone, although cellular damages were still observed at CAF and f-MWCNTs treatments. Increased biotransformation capacity at 18 °C and MIX treatment may explain lower caffeine concentration observed. At increased temperature differences among treatments were not so evident as at 18 °C, with a similar biological pattern among contaminated and control clams. Higher caffeine accumulation at MIX treatment under warming conditions may result from clams' inefficient biotransformation capacity when exposed to increased temperatures.

Coal mine effluent-induced metal bioaccumulation, biochemical, oxidative stress, metallothionein, and histopathological alterations in vital tissues of the catfish, Clarias batrachus.

In the present study, a multi-biomarker approach was used to assess the toxicity of the coal mine effluent (CME) generated at the Rajrappa coal mine on the catfish Clarias batrachus. A core of biomarkers indicative of nutritional value, oxidative stress, and histopathology was selected to illustrate the toxic effects of CME-containing different heavy metals and other toxicants. The results of metal bioaccumulation in CME-exposed fish tissues revealed the highest metal concentration in liver (1.34-297.68 mg/kg) while lowest in muscles (1.47-23.26 mg/kg) as compared to other tissues and so was the metallothionein level. The high value of bioaccumulation observed in liver, kidney, and gills reflects their affinity for metals. In addition, the values of metal pollution index (MPI) of different fish tissues further affirmed that liver followed by kidney and gills are at greater risk than brain, skin, and muscles. Significant alterations in the activity of certain enzymes (aspartate amino transferase, alanine amino transferase, alkaline phosphatase) as well as oxidative stress markers (superoxide dismutase, catalase and lipid peroxidation) were detected in the tissues of CME-exposed fish. The tissue-specific metal accumulation and increased metallothionein levels may be associated with the biochemical and physiological activity of an organ and its constitutive antioxidant defenses. The histopathological changes in the various tissues of the CME-exposed fish justify the high metal accumulation and biochemical alterations. Overall results indicate that the Rajrappa coal mine effluent is very toxic having adverse health impact on the fish and might also affect the human health when consumed.