Histotoxicity induced by copper oxide nanoparticles (CuO-NPs) on developing mice (Mus musculus).

The wide range of applications of nanoparticles (NPs) in various industries have led to serious consequences in terms of teratogenic toxicity. The aim of current work was to evaluate the teratogenic effects of copper oxide (CuO) nanoparticles in albino mice.In this experimental study, after mating, inseminated 40 female mice were divided randomly into 4 pools (1 control and 3 experimental), ten each. Doses were administered intravenously (We followed the protocol by Yaqub et al. (2018), intravenous application is faster route as compared to oral dosage)to all the experimental groups on the 6th day of gestation (GD), dose concentrations were 200, 133.3 and 100 mg/kg body weights respectively.The doses were prepared in sequence (1/2, 1/3, 1/4 0f LD50) according to already published work. The effects of CuO-NPs show linear relationship with the above sequence. The control group was administered only with distilled water.The gravid females were sacrificed through cervical disruption at the 18th day of gestation, fetuses were removed and divided into four sets (pools) for morphometric, morphological and histological studies. Data were subjected to statistical analysis by using Tukey's test in light of ANOVA at p < 0.05 level of significance. Findings of the present study showed that CuO-NPs various concentrations affect developmental abnormalities i.e.runt embryos, resorbed uteri, exencephaly, hygroma, macroglossia, micromelia, open eye, omphalocoel, scoliosis, kyphosis and kinked tail. It is concluded that exposure to CuO-NPs may potentially lead to the developmental deformities in mice.

Teratological effects of titanium dioxide nanoparticles in mice embryo.

Nanoparticles have numerous applications related to human uses. Titanium dioxide nanoparticles (TiO2-NPs) are extensively used in many daily utilities. The small size particles and larger uses in the industry have led them to become a threatening entity to the living organisms. The unchecked use and dumping in the environment poses a significant toxicological risk to the developing mammalian embryo. The present study was conducted to determine the developmental toxicity and teratogenic effects of TiO2-NPs in murine embryos. The TiO2-NPs were introduced intravenously into pregnant mice graded as T1 (0.52 mg/g BW), T2 (0.7 mg/g BW), and T3 (1.05 mg/g BW) along with control with no dose administration T0 (0.00 mg/g BW). Results recorded after 14 days were resorbed fetuses, dropped wrist, hemorrhages, sacral hygromas, and kinked tails. It was concluded that the exposure of TiO2-NPs in mentioned doses from any source may lead to deleterious effects on the development of an embryo.

Toxicological effects of toxic metals (cadmium and mercury) on blood and the thyroid gland and pharmacological intervention by vitamin C in rabbits.

Cadmium and mercury are non-biodegradable toxic metals that may cause many detrimental effects to the thyroid gland and blood. Vitamin C has been found to be a significant chain-breaking antioxidant and enzyme co-factor against metal toxicity and thus make them less available for animals. The current study was performed to find the effect of individual metals (cadmium and mercury), their co-administration, and the ameliorative effects of vitamin C on some of the parameters that indicate oxidative stress and thyroid dysfunction. Cadmium chloride (1.5 mg/kg), mercuric chloride (1.2 mg/kg), and vitamin C (150 mg/kg of body weight) were orally administered to eight treatment groups of the rabbits (1. control; 2. Vit C; 3. CdCl2; 4. HgCl2; 5. Vit C + CdCl2; 6. Vit C + HgCl2; 7. CdCl2 + HgCl2, and 8. Vit C + CdCl2 + HgCl2). After the biometric measurements of all experimental rabbits, biochemical parameters viz. triidothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), and triglycerides were measured using commercially available kits. The results exhibited significant decline (p < 0.05) in mean hemoglobin, corpuscular hemoglobin, packed cell volume, T3 (0.4 ± 0.0 ng/ml), and T4 (26.3 ± 1.6 ng/ml) concentration. While, TSH (0.23 ± 0.01 nmol/l) and triglyceride (4.42 ± 0.18 nmol/l) were significantly (p < 0.05) increased but chemo-treatment with Vit C reduces the effects of Cd, Hg, and their co-administration but not regained the values similar to those of controls. This indicates that Vit C had a shielding effect on the possible metal toxicity. The Cd and Hg also found to accumulate in vital organs when measured by atomic absorption spectrophotometer. The metal concentration trend was observed as follows: kidney > liver > heart > lungs. It was concluded that Cd and Hg are toxic and tended to bioaccumulate in different organs and their toxic action can be subdued by vitamin C in biological systems.

Renal toxicity of heavy metals (cadmium and mercury) and their amelioration with ascorbic acid in rabbits.

Cadmium and mercury are among the most toxic and dangerous environmental pollutants that may cause fatal implications. Vitamin C is an important chain-breaking antioxidant and enzyme co-factor against heavy metals. The objective of the present study was to evaluate the toxicological effects of cadmium chloride, mercuric chloride, and their co-administration on biochemical parameters of blood serum and metal bioaccumulation in kidneys and also to elucidate the protective effect of vitamin C in rabbits against these metals. In the current research, cadmium chloride (1.5 mg/kg), mercuric chloride(1.2 mg/kg), and vitamin C (150 mg/kg of body weight) were orally administered to eight treatment groups of the rabbits (1, control; 2, vitamin; 3, CdCl2; 4, HgCl2; 5, vitamin + CdCl2; 6, vitamin + HgCl2; 7, CdCl2 + HgCl2, and 8, vitamin + CdCl2 + HgCl2). After the biometric measurements of all experimental rabbits, biochemical parameters viz. creatinine, cystatin C, uric acid, and alkaline phosphatase (ALP) and metal bioaccumulation were determined using commercially available kits and atomic absorption spectrophotometer, respectively. The levels of creatinine (28.3 ± 1.1 µmol/l), cystatin C (1932.5 ± 38.5 ηg/ml), uric acid (4.8 ± 0.1 mg/day), and ALP (51.6 ± 1.1 IU/l) were significantly (P < 0.05) increased due to administration of mercuric chloride but in the presence of vitamin C, the effects of mercuric chloride on creatinine (21.9 ± 1.4 µmol/l), cystatin C (1676.2 ± 42.2 ηg/ml), uric acid (3.9 ± 0.1 mg/day), and ALP (43.3 ± 0.8 IU/l) were less as compared to metal-exposed specimens. Similar results were found in rabbits treated with cadmium chloride and vitamin C and also with co-administration of both metals and vitamin C. Because of the bio-accumulative nature of cadmium chloride and mercuric chloride, these metals were accumulated in kidneys of rabbits, which might lead to deleterious effects. The results of the present study provide an insight into the toxicity of the cadmium chloride, mercuric chloride, and/or their combination on biochemical parameters as well as kidneys of the rabbits and the ameliorating potential of vitamin C against these metals is also evaluated.