Histopathological and Biochemical Comparative Study of Copper Oxide Nanoparticles and Copper Sulphate Toxicity in Male Albino Mice Reproductive System.

Copper (Cu) is an essential trace element for the efficient functioning of living organisms. Cu can enter the body in different ways, and when it surpasses the range of biological tolerance, it can have negative consequences. The use of different nanoparticles, especially metal oxide nanoparticles, is increasingly being expanded in the fields of industry and biomedical materials. However, the impact of these nanoparticles on human health is still not completely elucidated. This comparative study was conducted to evaluate the impacts of copper oxide nanoparticles (CuO NPs) and copper sulphate (CuSO4 0.5 (H2O)) on infertility and reproductive function in male albino mice BALB/c. Body weight, the weight of male reproductive organs, malondialdehyde (MDA) level, caspase-3 level, and the presence of Ki67 and CD68, as detected using the amino-histochemistry technique, were investigated. Animals were treated with 25 and 35 mg/kg of CuO NPs and CuSO4 0.5 (H2O) by oral gavage for 14 days. The control group was given distilled water by oral gavage. Body weight significantly decreased at the end of experiments in both treated groups in a concentration- and time-dependent manner compared with the control group. Weights of testes and epididymis (head and tail), as well as the weight of the seminal vesicle, showed a significant decrease compared with the control. However, the average weights of the seminal vesicle and prostate significantly increased. Caspase-3 and MDA levels increased in the CuO NP and CuSO4 0.5 (H2O) groups compared with the control group, and there was a significant difference between the two concentrations used. Immunohistochemical results detected a significant decrease in Ki67 protein in the treatment groups compared with the control. However, increase in CD68 protein was found in groups treated with CuO NPs and CuSO4 0.5 (H2O) compared with the control group. Overall, this in vivo comparative study of CuO NPs and CuSO4 0.5 (H2O) showed that oral intake of copper NPs at 25 and 23 mg/kg was safer to the mice reproductive system than CuSO4 0.5 (H2O) at the same dose. CuSO4 0.5 (H2O) significantly influenced the histopathological and toxicological alteration responses.

Sublethal effects of copper sulphate compared to copper nanoparticles in rainbow trout (Oncorhynchus mykiss) at low pH: physiology and metal accumulation.

A few studies have investigated the interaction between copper toxicity and water pH in fishes, but little is known about the effects of acidic pH on the toxicity of copper nanoparticles (Cu-NPs). This study aimed to describe the sub-lethal toxic effects of Cu-NPs compared to CuSO4 at neutral and acidic water pH values in juvenile rainbow trout. Fish were exposed in triplicate (3 tanks/treatment) to control (no added Cu), or 20µgl(-1) of either Cu as CuSO4 or Cu-NPs, at pH 7 and 5 in a semi-static aqueous exposure regime for up to 7 days. Acidification of the water altered the mean primary particle size (at pH 7, 60±2nm and pH 5, 55±1nm) and dialysis experiments to measure dissolution showed an increased release of dissolved Cu from Cu-NPs at pH 5 compared to pH 7. Copper accumulation was observed in the gills of trout exposed to CuSO4 and Cu-NPs at pH 7 and 5, with a greater accumulation from the CuSO4 treatment than Cu-NPs at each pH. The liver also showed Cu accumulation with both Cu treatments at pH 7 only, whereas, the spleen and kidney did not show measurable accumulation of Cu at any of the water pH values. Exposure to acid water caused changes in the ionoregulatory physiology of control fish and also altered the observed effects of Cu exposure; at pH 5, branchial Na(+)/K(+)-ATPase activity was greater than at pH 7 and the inhibition of Na(+)/K(+)-ATPase activity caused by exposure to CuSO4 at pH 7 was also not observed. There were some changes in haematology and depletion of plasma Na(+) at pH 7 and 5 due to Cu exposure, but there were few material-type or pH effects. Overall, the data show that the accumulation of Cu is greater from CuSO4 than Cu-NPs; however, understanding of the effects of low pH on bioavailability of CuSO4 may not be directly transferred to Cu-NPs without further consideration of the physico-chemical behaviour of Cu-NPs in acid water.

Critical comparison of intravenous injection of TiO2 nanoparticles with waterborne and dietary exposures concludes minimal environmentally-relevant toxicity in juvenile rainbow trout Oncorhynchus mykiss.

A critical comparison of studies that have investigated tissue accumulation and toxicity of TiO2-NPs in fish is necessary to resolve inconsistencies. The present study used identical TiO2-NPs, toxicological endpoints, and fish (juvenile rainbow trout Oncorhynchus mykiss) as previous studies that investigated waterborne and dietary toxicity of TiO2-NPs, and conducted a critical comparison of results after intravenous caudal-vein injection of 50 µg of TiO2-NPs and bulk TiO2. Injected TiO2-NPs accumulated only in kidney (94% of measured Ti) and to a lesser extent in spleen; and injected bulk TiO2 was found only in kidney. No toxicity of TiO2 was observed in kidney, spleen, or other tissues. Critical comparison of these data with previous studies indicates that dietary and waterborne exposures to TiO2-NPs do not lead to Ti accumulation in internal tissues, and previous reports of minor toxicity are inconsistent or attributable to respiratory distress resulting from gill occlusion during waterborne exposure.

Histopathological effects of waterborne copper nanoparticles and copper sulphate on the organs of rainbow trout (Oncorhynchus mykiss).

It is unclear whether copper nanoparticles are more toxic than traditional forms of dissolved copper. This study aimed to describe the pathologies in gill, gut, liver, kidney, brain and muscle of juvenile rainbow trout, Oncorhynchus mykiss, exposed in triplicate to either a control (no added Cu), 20 or 100 µg l(-1) of either dissolved Cu (as CuSO(4)) or Cu-NPs (mean primary particle size of 87 ± 27 nm) in a semi-static waterborne exposure regime. Fish were sampled at days 0, 4, and 10 for histology. All treatments caused organ injuries, and the kinds of pathologies observed with Cu-NPs were broadly of the same type as CuSO(4) including: hyperplasia, aneurisms, and necrosis in the secondary lamellae of the gills; swelling of goblet cells, necrosis in the mucosa layer and vacuole formation in the gut; hepatitis-like injury and cells with pyknotic nuclei in the liver; damage to the epithelium of some renal tubules and increased Bowman's space in the kidney. In the brain, some mild changes were observed in the nerve cell bodies in the telencephalon, alteration in the thickness of the mesencephalon layers, and enlargement of blood vessel on the ventral surface of the cerebellum. Changes in the proportional area of muscle fibres were observed in skeletal muscle. Overall the data showed that pathology from CuSO(4) and Cu-NPs were of similar types, but there were some material-type effects in the severity or incidence of injuries with Cu-NPs causing more injury in the intestine, liver and brain than the equivalent concentration of CuSO(4) by the end of the experiment, but in the gill and muscle CuSO(4) caused more pathology.

Subtle alterations in swimming speed distributions of rainbow trout exposed to titanium dioxide nanoparticles are associated with gill rather than brain injury.

The effects of engineered nanomaterials on fish behaviours are poorly understood. The present study aimed to determine the locomotor behaviours of trout during waterborne exposure to titanium dioxide nanoparticles (TiO(2) NPs) as well as inform on the underlying physiological mechanisms involved. Trout were exposed to either control (without TiO(2)), 1 mg l(-1) TiO(2) NPs or 1 mg l(-1) bulk TiO(2) for 14 days. Titanium dioxide exposure resulted in 31 (bulk) and 22 fold (nano) increases in the Ti concentrations of gill tissue compared to controls, but there were no measurable increases of Ti in the internal organs including the brain. Gill pathologies were observed in both TiO(2) treatments. Locomotor behaviours were quantified using video tracking software and the proportion of time spent swimming at high speed (>20 cms(-1)) was significantly decreased in fish exposed to TiO(2) NPs, compared to controls, but not fish exposed to bulk TiO(2). The shift in swimming speed distribution in the TiO(2) NP-exposed fish was associated with decreased area of red pulp in the spleen, increases in haematocrit and whole blood haemoglobin, all consistent with a compensation for respiratory hypoxia without the accumulation of plasma lactate. Fish exposed to TiO(2) NPs also retained competitive abilities when paired with controls in aggressive social encounters. The duration of competitive contests, the level of aggression and contest outcome were not affected by NP exposure. Neurological injury did not explain the changes in locomotor behaviour, although there was some apparent enlargement of the blood vessels on the brain. Whole brain homogenates showed a statistically significant increase in oxidative stress defences such as the total glutathione pool, but without loss of Na(+)K(+)-ATPase or acetylcholinesterase activities.