Investigating the impact of different routes of nano and micro nickel oxide administration on rat kidney architecture, apoptosis markers, oxidative stress, and histopathology.

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.

The Ameliorative Effect of Naringenin on Fenamiphos Induced Hepatotoxicity and Nephrotoxicity in a Rat Model: Oxidative stress, Inflammatory markers, Biochemical, Histopathological, Immunohistochemical and Electron Microscopy Study.

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.

Subacute exposure to dimethoate induces hepatotoxic and nephrotoxic effects on male rats: Ameliorative effects of ferulic acid

Dimethoate commonly used as environmental ares for control pests which is widely used throughout in the world and itcaused toxic effects on nontarget organisms especially mammalian. Ferulic acid is known to protective compound generally used in toxicology studies. Thus, inthis study, we investigatedthe protective role of ferulic acid against the possible toxic effects of low and high doses of dimethoate. Male rats were randomly divided into six groups: control; ferulic acid; low and high dose dimethoate; both ferulic acid and low dose dimethoate; both ferulic acid and high dose dimethoate. The dimethoate treatment to rats caused oxidative stress in liver and kidney tissue via increased malondialdehyde levels and changes in superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase activities. All dose dimethoate treatments also caused histopathological alterations and differences in activities in alanine aminotransferase, aspartate aminotransferase, total protein, albumin, lactate dehydrogenase, total cholesterol, urea, uric acid, and creatinine levels. The histopathological results verified the biochemical findings for both liver and kidney. Co-administration of ferulic acid with dimethoate improved antioxidative parameters and eased some biochemical parameters mentioned above. Ferulic acid was also seen to play a beneficial role in the histopathological effects of dimethoate for both liver and kidney.

Antioxidant Status, Lipid Peroxidation and Testis-histoarchitecture Induced by Lead Nitrate and Mercury Chloride in Male Rats

ABSTRACT This study was done to evaluate the effects of lead nitrate and mercury chloride in testis tissues of Wistar rats. Lead nitrate and mercury chloride are widely used heavy metals in industry. Oral lead and mercury administrations to adult male rats at doses 45 mg/kg bw and 0.02 mg/kg bw, respectively for 4 weeks caused a significant increasing in MDA levels and antioxidant enzyme activities (SOD, CAT, GPx and GST). The MDA levels and acivities of antioxidant enzymes was lower in rats that were administrated by lead nitrate than mercury chloride treated group. Light microscopic analyses revealed that lead nitrate and mercury chloride induced numerous histopathological changes in testis tissues of rats. Histopathological observations of the testis tissues showed that mercury chloride caused more harmful effects than lead nitrate, too. The results indicate that lead nitrate and mercury chloride have reproductive toxicity, in male rats at the tested doses. The effect which we observed applying the lead nitrate and mercury chloride together, was more greater than when we used them alone.

Lead Nitrate Induced Testicular Toxicity in Diabetic and Non-Diabetic Rats: Protective Role of Sodium Selenite

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.