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Considering that the involvement of reactive oxygen species (ROS) has been implicated in the toxicity of various pesticides, this study was designed to study the ameliorative effect of Vitamin E (100 mg/kg body weight) on mice (25 - 30 mg) treated with diazinon (32.5 or 16.25 mg/kg body weight) organophosphate insecticide for 14 days. Subchronic DZN exposure and the protective effects of vitamins E (vitE) were evaluated for their effects on haematological indices, the enzymes concerning liver damage [plasma alanine aminotransferase (ALT), aspartate aminotaransferase (AST), alkaline phosphatise (AIP), and some parameters of kidney function (urea and creatinine) in mice. Additionally, the histopathological changes in liver and kidney tissue were examined. The high dose of diazinon (DZNH) decreased the body weight significantly at the end of experiment. Additionally, the liver and kidney were examines for histopathological changes. The high dose of diazinon decreased body weight significantly. Moreover, there was a statistically significant decrease in haemoglobin (Hb), red blood cell (RBC) and hematocrit (Hct) in diazinon-treated mice compared to controls. This decrease was partially remedied in the diazinon-treated group that also received vitE. Damage in the liver and kidney tissues was also evident as elevated plasma ALT, AST, ALP, urea and creatinine. VitE partially counteracts the toxic effect of DZN and repairs tissue damage in the liver and kidney, especially when supplemented to 1/4 LD50 intoxicated animals. Histopathological changes in liver and kidney were observed only in 32.5 mg/kg DZN given group. These results suggest that the effects of DZN are dose dependent. No pathological findings were observed in vitE + DZN treated groups. According to the present study, we conclude that vitE can reduce the detrimental impacts of diazinon on haematological indicies, as well as liver and kidney function.

Aspartame (ASP) has been used as an alternative to sucrose for diabetics and obese people worldwide. Co-administration of L-carnitine (LC) with ASP has a protective effect against the liver and kidney toxicity induced of ASP. The goal of the investigation was to assess the enhancement of LC effect on the cardiac toxicity caused of ASP. The rats were divided into 6 groups: control with saline, LC (10 mg/kg), ASP (75 mg/kg), ASP (150 mg/kg), LC with 75 mg/kg of ASP, and LC with 150 mg/kg ASP. The antioxidants were determined by measuring the activities of myeloperoxidase, xanthine oxidase, superoxide dismutase, catalase, and glutathione peroxidase, and by assessing the levels of lipid peroxidation, total thiols, and glutathione. There was a significant elevation in LPO, in conjunction with a significant decline in the enzymatic antioxidants superoxide dismutase, catalase, and glutathione peroxidase and the non-enzymatic antioxidants glutathione and thiols. The cardiac myofibrils were found in a disarrayed pattern in ASP treated-animals as compared to the control rats. The animals treated with ASP-HD showed more than one apoptotic cell with a large tail and a small head, and the relaxed loops of the damaged DNA were extended to form a comet-shaped structure. These effects may be due to the excessive generation of reactive oxygen species by ASP, which reduces cardiac function. Co-administration of LC with ASP improved all of the above-mentioned parameters that were disrupted of ASP alone. This study evidences a sufficient originality in showing how LC plays a positive role against cardiac toxicity of ASP.

Background Aspartame (ASP) is used for treatment of obesity and diabetes mellitus. This study was designed to illustrate the biochemical responses and histopathological alterations besides the genotoxicity of ASP alone or with l-carnitine (LC) in the liver of rats. Methods Animals were separated into six groups: control, lower dose of ASP (ASP-LD; 75 mg/kg), higher dose of ASP (ASP-HD; 150 mg/kg), l-carnitine (LC; 10 mg/kg), ASP-LD plus LC, and ASP-HD plus LC. Treatment was carried out orally for 30 consecutive days. Results ASP raised the activity of some enzymes of liver markers and disturbed the lipid profile levels. The hepatic reduced glutathione (GSH) levels, the marker enzymes of antioxidant activities, were obviously diminished, and, possibly, the lipid peroxidation, C-reactive protein, and interleukins levels were increased. ASP significantly increased the DNA deterioration in comparison with the control in a dose-dependent manner. LC prevented ASP-induced liver damage as demonstrated by the enhancement of all the above parameters. Results of histopathological and electron microscopic examination proved the biochemical feedback and the improved LC effect on liver toxicity. Conclusions The co-treatment of LC showed different improvement mechanisms against ASP-induced liver impairment. So, the intake of ASP should be regulated and taken with LC when it is consumed in different foods or drinks to decrease its oxidative stress, histopathology, and genotoxicity of liver.

The present study aimed to investigate the effect of the royal jelly (RJ) on hepatotoxicity induced by molybdenum nanoparticles (MoO3-NPs), cadmium chloride (CdCl2), or their combination in male rats at biochemical, inflammation, immune response, histological, and ultrastructural levels. The physicochemical properties of MoO3-NPs have been characterized, as well as their ultrastructural organization. A rat experimental model was employed to assess the liver toxicity of MoO3-NPs, even in combination with CdCl2. Different cellular studies indicate divergent mechanisms, from increased reactive oxygen species production to antioxidative damage and cytoprotective activity. Seventy male rats were allocated to groups: (i) control; (ii) MoO3-NPs (500 mg/kg); (iii) CdCl2 (6.5 mg/kg); (iv) RJ (85 mg/kg diluted in saline); (v) MoO3-NPs followed by RJ (30 min after the MoO3-NPs dose); (vi) CdCl2 followed by RJ; and (vii) a combination of MoO3-NPs and CdCl2, followed by RJ, for a total of 30 successive days. Hepatic functions, lipid profile, inflammation marker (CRP), antioxidant biomarkers (SOD, CAT, GPx, and MDA), and genotoxicity were examined. Histological changes, an immunological marker for caspase-3, and transmission electron microscope variations in the liver were also investigated to indicate liver status. The results showed that RJ alleviated the hepatotoxicity of MoO3-NPs and/or CdCl2 by improving all hepatic vitality markers. In conclusion, the RJ was more potent and effective as an antioxidant over the oxidative damage induced by the combination of MoO3-NPs and CdCl2.

Diabetes mellitus (DM) causes an imbalance in the oxidative status of the human body. Three novel Dapagliflozin (Dapg) Zn (II), Cr (III) and Se (IV) complexes were prepared and characterized by elemental analysis, IR, electronic spectra, magnetic susceptibility, scanning electron microscopy (SEM) and X-ray diffraction. The molar conductance values confirmed the non-electrolytic nature of the Dapg complexes. According to spectral data, Dapg acts as a bidentate ligand. The thermal analyses of the complexes were studied using the DSC technique. The surface morphology and particle sizes of the Dapg complexes were investigated using SEM and XRD. XRD confirmed the crystalline structure for the complexity. This study investigated the effect of novel metal complexes of Dapg with the metals Zn (II), Cr (III) and Se (IV) on oxidative injury and tissue damage in the hepatic tissue of streptozotocin (STZ)-induced diabetic male rats. DM was experimentally induced in male rats. The diabetic rats received Dapg, Dapg/Zn, Dapg/Cr and Dapg/Se orally for 30 successive days. Male rats exposed to STZ showed multi-histopathological alterations in their hepatic tissue, including inflammatory and structural changes. STZ elevated oxidative stress markers in the hepatic tissue and lowered the antioxidant defense enzymes. Supplementation of Dapg with Zn, Cr or Se novel complexes significantly prevented hepatic injury and suppressed the generation of reactive oxygen species. The Dapg/Zn complex was highly effective against Bacillus subtilis and Streptococcus penumonia, while Dapg/Cr was highly effective against Escherichia coli and Pseudomonas aeruginosa, and Dapg/Se was highly effective against Staphylococcus aureas. In conclusion, Dapg novel metal complexes with Zn, Cr or Se protect against oxidative injury and the pathophysiological and bacterial complications of DM and hepatic tissue injury. The Dapg novel metal complexes improved hepatic functions, reduced blood glucose levels and enhanced the levels of antioxidant defense enzymes in diabetic male rats.

Background: Nanotechnology application has widespread use in many products. Copper nanoparticles (CuNPs) are widely used in industrial applications. The present study was conducted to investigate the effect of the ethanolic saffron extract (ESE) as a natural antioxidant on the hepatotoxicity induced by CuNPs in male mice. Methods: The characterization of CuNPs was determined using ultraviolet–visible absorption spectroscopy, particle size analysis, zeta potential, Fourier-transform infrared spectroscopy, and electron microscope. The effect of saffron on the hepatotoxicity induced by CuNPs in mice was evaluated by evaluating the survival rate of the mice, oxidative stress, antioxidant capacity, DNA evaluation, as well as its effect on the histology and transmission electron microscope of the liver. Results: The results revealed that all parameters were affected in a dose-dependent manner by CuNPs. These effects have been improved when the treatment of CuNPs is combined with ethanolic saffron extract. Conclusions: We can conclude that saffron and its bioactive crocin portion can prevent CuNP-induced oxidative liver damage. This substance should be useful as a new pharmacological tool for oxidative stress prevention.

Acetamiprid (neonicotinoid insecticide) and azoxystrobin (fungicide) are widespread pesticides used for pest management, but they have the potential for toxicity to mammals. The goal of this study was to look for oxidative stress, metabolic alterations, and reproductive problems in male rats’ serum after 2 months of exposure to sub-lethal dosages of acetamiprid and azoxystrobin. Seven classes of male rats were formed: control, 3 groups of acetamiprid (1/10, 1/20, 1/40 LD50), and 3 groups of azoxystrobin (1/10, 1/20, 1/40 LD50) and were orally daily treated (n = 8/group). Our findings revealed that acetamiprid and azoxystrobin disrupted oxidative and metabolic processes in the examined rats throughout 30 and 60 days of testing. The levels of nitric oxide increased significantly, while catalase, a superoxide dismutase enzyme, and glutathione reductase activity were reduced. Serum levels of sex hormones, calcium, and total protein have all dropped substantially in rats. In comparison to the control group, the testis and liver structure, as well as spermatozoa parameters, had distinct histological characteristics. In conclusion, acetamiprid and azoxystrobin exhibit dose- and time-dependent effects on oxidative parameters that cause testis damage.