ABSTRACT
Fenamiphos (FNP) is an organophospate pesticide that causes many potential toxicities in non-target organisms. Naringenin (NAR) has protective properties against oxidative stress. In this study, FNP (0.76 mg/kg bw) toxicity and the effect of NAR (50 mg/kg bw) on the liver and kidney of rats were investigated via biochemical, oxidative stress, immunohistochemical, cytopathological and histopathologically. As a result of biochemical studies, FNP caused oxidative stress in tissues with a change in total antioxidant/oxidant status. After treatment with FNP, hepatic and renal levels of AChE were significantly reduced while 8-OHdG and IL-17 levels, caspase-3 and TNF-α immunoreactivity increased compared to the control group. It also changed in serum biochemical markers such as ALT, AST, BUN, creatinine. Exposure to FNP significantly induced cytopathological, histopathological and immunohistochemical changes through tissue damage. NAR treatment restored biochemical parameters, renal/hepatic AChE, ultrastructural, histopathological and immunohistochemical changes modulated and blocked the increasing effect of FNP on tissues caspase-3 and TNF-α expressions, 8-OHdG and IL-17 levels. In electron microscopy studies, swelling was observed in the mitochondria of the cells in both tissues of the FNP-treated rats, while less ultrastructural changes in the FNP plus NAR-treated rats.
ABSTRACT
Although the production and use of nickel oxide nanoparticles (NiONP) are widespread, environmental and public health problems are associated with it. The kidney is the primary organ in excretion and is among the target organs in nanoparticle toxicity. This study aimed to compare the renal toxicity of nickel oxide (NiO) microparticles and nickel oxide nanoparticles by different routes of administration, such as oral, intraperitoneal (IP), and intravenous (IV). Seven groups were formed, with 42 male rats and six animals in each group. NiO oral (150 mg/kg), NiO IP (20 mg/kg), NiO IV (1 mg/kg), NiONP oral (150 mg/kg), NiONP IP (20 mg/kg), and NiONP IV (1 mg/kg) was administered for 21 days. After NiO and NiONP administration, a decrease in antioxidant activities and an increase in lipid peroxidation occurred in the kidney tissue of rats. Increased kidney urea, uric acid, and creatinine levels were observed. Inhibition of acetylcholinesterase activity and an increase in interleukin 1 beta were detected. Apoptotic markers, Bax, caspase-3, and p53 up-regulation and Bcl-2 down-regulation were observed. In addition, histopathological changes occurred in the kidney tissue. In general, it was observed that nickel oxide microparticles and nickel oxide nanoparticles cause inflammation by causing oxidative stress in the kidney tissue, and NiONP IV administration is more effective in renal toxicity.
ABSTRACT
BACKGROUND: Nickel oxide nanoparticles (NiONPs) are used as industrial photoelectric and recording materials, catalysts, and sensors. It has been increasingly used in many industrial sectors. Lungs are the important biological barrier that comes into contact with nanomaterials in the inhaled air. This study aimed to compare the effects of nickel oxide (NiO) microparticles and NiONPs on rat lung tissues in different dose administrations, such as oral, intraperitoneal, and intravenous. METHODS: The mature male Wistar rats (n = 42) were divided into seven groups with six animals: Group I (control), Group II NiO gavage (150 mg/kg), Group III NiO intraperitoneally (20 mg/kg), Group IV NiO intravenously (1 mg/kg), Group V NiONP gavage (150 mg/kg), Group VI NiONP intraperitoneal (20 mg/kg), and Group VII NiONP intravenous (1 mg/kg) for 21 days. Oxidative stress (MDA, CAT, SOD, GPx, and GST), apoptotic marker (p53) gene expression, and histopathological changes were determined comparatively. RESULTS: Our data showed that NiO and NiONPs caused an exposure-related increase in the incidence of alveolar/bronchiolar pathological changes, oxidative damage, and p53 gene expression in male rats. Intravenous exposure to NiONPs produces statistically (p < 0.05) more oxidative damage and histopathological changes than exposure to NIO. It also induces higher upregulation of the pro-apoptotic p53 gene. CONCLUSION: NiO and NiONPs induce oxidative damage, histopathological alterations and p53 gene expression in rat lungs. Thus, exposure to NiO and NiONPs, especially intravenously, may indicate more toxicity and carcinogenicity.
Subject(s)
Nanoparticles , Nickel , Tumor Suppressor Protein p53 , Rats , Male , Animals , Rats, Wistar , Lung , Apoptosis , Nanoparticles/toxicity , Oxidative StressABSTRACT
Among heavy met als, lead is one of the common pollutants found in the environment and biological system. In the present study, streptozotocin-induced diabetic and normal non-diabetic male Wistar rats were given sodium selenite (1.0 mg/kg bw), lead nitrate (22.5 mg/kg bw) and sodium selenite plus lead nitrate (1.0 mg/kg+22.5 mg/kg bw, respectively) through gavage. At the end of 4th week, malondialdehyde (MDA) levels, antioxidant enzyme activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST)], and histopathological changes of testes were investigated compared to the control group. No significant differences were observed between the control and sodium selenite treated groups. However, lead nitrate increased the levels of MDA, SOD, CAT, GPx and GST activities compared with the control group in diabetic and non-diabetic rats. Light microscopic analyses revealed that lead nitrate induced numerous histopathological changes in testis tissues of diabetic and non-diabetic rats. In the diabetic and non-diabetic sodium selenite plus lead nitrate treated groups, there were statistically significantly decreased MDA levels and antioxidant enzymes activities and mild pathological changes. As a result, sodium selenite significantly reduced lead nitrate induced testicular toxicity for both diabetic and non-diabetic rats.