Objective. To study the effects of deoxynivalenol (DON) on the liver in male mice.Methods. DON being administered by intraperitoneal injection (8.8 and 17.5 mg/kg b. w.). Lactobacillus reuteri and Lactobacillus gasseri were also administered to investigate their protective activity against DON-induced hepatic damage in mice. Results. It was observed that, serum ALT, AST, and ALP levels were significantly increased in DON-treated mice as compared with those in the control group (P 0.05). When mice were treated with DON and L. reuteri or L. gasseri, significant reduction was noticed in serum AST, ALT and ALP at P 0.05 as compared to DON treated group. Liver sections of mice received DON showed severe degeneration of the parenchyma; the hepatocyte plates were disrupted, the cells were swollen and vacuolated, and some signs of fatty degeneration were observed. Administration of oral doses of Lactobacillus reuteri and Lactobacillus gasseri for seven consecutive days followed by a single dose of DON (8.8 and 17.5 mg/kg b.w.) respectively revealed that liver has still its normal structure, except for the development of focal necrosis in case of using Lactobacillus reuteri. Conclusion. The present study indicates that probiotics bacteria, Lactobacillus reuteri and Lactobacillus gasseri, could play a protective role against the hepatotoxic effects induced in the liver by DON.

Objective: In present study the effect of the organophosphorus insecticide, profenofos, on the antioxidant enzymes activities and mucosa of stomach was investigated in rats. Material & Methods: To evaluate these effects,the biochemical, histological, morphometrical, and histochemical studies on stomach were done. Animals were divided into three groups 10 animals of each. Control animals (group I)were administered vehicle. Treatment group animals (group II and III) were respectively administered oral doses of profenofos: 86.8 and 214.4 mg/kg b. wt. daily for 15 days. Results: The administration of profenofos caused a significant decrease in the levels of superoxide dismutase (SOD),glutathione peroxidase (GPx) and reduced glutathione (GSH), and an increase in the lipid peroxidation (LPO) level (p 0.05). The histopathological findings indicated that profenofos caused different alterations in stomach, including haemorrhagic areas in the mucosa and submucosa and degenerative changes. The histochemical examination showed noticeable reduction in polysaccharide materials of stomach; the cells of such organ displayed faint stain. Conclusion: Generally, profenofos caused extensive biochemical, histological, and histochemical injury. Such effects were relevant to the amount of dose given.

The present study was designed to investigate the potential protective effect of melatonin against the hepatic and renal toxicity of lead in male rats. Three groups of animals were used in this study (control, lead acetate-treated (100 mg/kg), and lead acetate plus melatonin (10 mg/kg) for 30 days. Levels of lipid peroxidation (LPO) products, superoxide dismutase (SOD) activity, total glutathione (GSH), histopathological changes in the liver and kidneys were investigated. In addition, nuclear area (NA), nuclear volume (NV) and the ratio of nuclear volume/cellular volume (N/C) were measured in the liver. The results revealed increased LPO and decreased SOD, GSH, NA, NV and N/C in the studied organs of lead-treated rats. Histopathological observations showed severe damage in the liver and kidneys. Melatonin co-treatment to the lead-administered rats attenuated the increase of LPO and restored the activity of SOD and levels of GSH as well as the mean values of NA, NV and N/C. Also, the morphological damage in the liver and kidneys was reduced and the tissues appeared like those of controls. The present study suggests that melatonin may be useful in combating free radical-induced damage due to lead toxicity.

The present study was designed to investigate the potential protective effects of melatonin on potassium dichromate (K2Cr2O7)(hexavalent chromium) induced nephrotoxicity in adult male rabbits. Animals were randomly divided into four experimental groups. The first group received saline solution daily for 30 days. The second group received melatonin at a dose of 10 mg/kg b.w./day. The third group was treated with 0.4 mg/kg b.w. K2Cr2O7.The fourth groupwas treated with 0.4 mg/kg b.w. K2Cr2O7 plus 10 mg/kg b.w. melatonin. Results showed normal kidney tissue and normal kidney functions in the first two groups. Histopathological observations of the third group showed structural abnormalities in the renal cortex including glomeruli and tubules. Histomorphometric study in the third group revealed significant decreased of the mean values of glomerulus area and glomerulus diameter, while, the mean percentage of the glomerular affection and tubules lumen area showed significant increased. Biochemical results of the third group showed significant increased of the levels of serum urea and creatinine. Melatonin co-treatment to the chromium-administered rabbits attenuated the increase of urea and creatinine and also improved the histopathological and histomorphometrical changes in the kidneys. The present study suggests that melatonin may be useful in ameliorate kidney damage due to chromium toxicity.

Paraquat is highly toxic compound for humans and animals. It has been used widely in agriculture as herbicide. The present study was designed to investigate the potential protective effect of Coenzyme Q10 against the hepatotoxicity of paraquat in male rats. The experiment was carried out using 24 male albino rats. Four groups of animals were used in this study: control, Coenzyme Q10 (10 mg/kg), paraquat-treated (9 mg/kg b.w), paraquat along with Coenzyme Q10 for 4 weeks. Light microscopic observations revealed that the hepatic tissue of control and Coenzyme Q10 groups showed normal hepatocytes structure. Histopathological observations of paraquat treated group showed severe damage in liver tissue such as hepatocytes degeneration and necrosis, congestion of blood vessels and hemorrhage. Biochemical studies indicated that serum Alanine aminotransferase (ALT), Aspartate aminotransferase (AST) and Alkaline Phosphatase (ALP) levels were elevated in paraquat treated group. Administration of paraquat significantly increased hepatic malondialdehyde (MDA) levels. Superoxide dismutase (SOD) activity and Glutathione (GSH) content in the liver of the paraquat administered rats were significantly decreased as compared with control group. Paraquat treated rats showed negative immunoreactivity to Alfa Fetoprotein (AFP) in the cytoplasm of the liver cells. Coenzyme Q10 administration attenuated the damages induced by paraquat in the liver of rats. The results of the present study indicated that Coenzyme Q10 has protective effect against liver damage induced by paraquat.

The present study was designed to investigate the potential protective effect of Coenzyme Q10 against the testicular toxicity of cadmium in male rabbits. Four groups of animals were used in this study (control, Coenzyme Q10, cadmium chloride-treated (5 mg/kg), cadmium chloride plus Coenzyme Q10 (10 mg/kg) for 30 days). Results showed normal testicular tissue in control and coenzyme Q10 groups. Histopathological observations of cadmium chloride group showed severe damage in testicular tissue such as atrophy in many seminiferous tubules, vacuolations and cellular debris. The germinal epithelium was sloughed off and the spermatogenic cell layers were disturbed. Morphometrical data displayed significant decrease in both seminiferous tubules diameter and the counted number of the different spermatogenic cells. Additionally, testosterone and luteinizing hormones level were decreased. Coenzyme Q10 co-treatment to the cadmiumadministered rabbits reduced testis histopathological changes and increased the levels of testosterone and luteinizing hormones. The present study suggests that coenzyme Q10 may be ameliorate testicular damage due to cadmium toxicity.

Doxorubicin is a highly effective antineoplastic agent, but it is well known for its oxidative damage to various body organs such as nephrotoxicity. The present study aimed to investigate the possible protective role of the natural antioxidant wheat germ oil on Doxorubicin -induced kidney toxicity. Studies were performed on four groups of mice. Control group, wheat germ oil group (100 mg/kg b.w.), Doxorubicin group (2.5 mg/kg/day) for seven days, and doxorubicin plus wheat germ oil group. Histopathological examination of kidney sections revealed that doxorubicin caused glomerular congestion with wide Bowman’s space and widened tubular lumen. Immunohistochemical localization of Caspase-3 for apoptosis was performed. Doxorubicin treated animals showed positive reaction to Caspase 3 in glomerulii and renal tubules as compared with controls. Administration of wheat germ oil reversed kidney damage with a marked reduction in tubular damage and apoptosis induced by doxorubicin.These results have suggested that wheat germ oil ameliorated doxorubicin -induced nephrotoxicity in male mice.

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The present study was directed to evaluate the toxic effects of orally administered titanium dioxide naonparticles (TiO2) on liver of male albino rats and to evaluate the ameliorative effects of N-acetylcysteine (NAC). Forty adult male albino rats were divided into 4 groups; control group, NAC group, TiO2 group and TiO2/ NAC group. Rats were administered either TiO2 (1200 mg kg-1 BW) or NAC (100 mg kg-1 BW) alone or together for 9 months. Blood was taken to evaluate serum changes in GPT, GOT and MDA levels. Liver tissues were examined for changes in MDA, GSH and changes in liver histopathology.Administration of TiO2 increased serum GPT, GOT and decreased MDA levels. Co-treatment of rats with NAC and TiO2 improved such significant changes induced by TiO2 alone. Moreover, significant time dependent increase in MDA and decrease in GSH levels in liver tissues were recorded. Liver histopathology showed vacuolar, hydropic degeneration and cell death of some hepatic cells. In conclusion, results confirmed the protective effect of NAC in amelioration of the biohazard effects induced by TiO2 in rats.

This study was done on 14 buffalo's adrenal glands. The adrenal gland of buffalo consisted of outer cortex and inner medulla. It was surrounded by thick CT capsule. The thickness of the capsule varied according to the age of the animals. It was thin (242.6 ± 12.1 μm) in young and thick (265.3 ± 13.2 μm) in adult animals. Thin septa extended into the parenchyma of the gland. The cortex consisted of three distinct zones, zona glomuralis (Arcuata) which was (385.5 ± 13.9 μm) in young animals while (415.7 ± 14.6 μm) in adult animals. The columnar cells of the arcuata contained numerous round mitochondria and smooth endoplasmic reticulum , while few rough endoplasmic reticulum. Zona fasiculata, which was the widest zone of the gland (865.6 ± 17.5 μm) in young animals while (912.8 ± 18.3 μm) in adult animals. The cuboidal cells of the zona fasiculata showed numerous round and oval mitochondria , small round electron-lucent lipid droplets , well developed Golgi complex and smooth endoplasmic reticulum. Zona reticularis which was (432.2 ± 14.3 μm) in young animals while (471.3 ± 15.8 μm) in adult animals. The cells contained round mitochondria, Golgi complex and less vacuole.The medulla was consisted of outer part that separated from the cortex by CT capsule. The thickness of the medulla was (457.8 ± 15.2 μm) in young animals while (482.5 ± 16.6 μm) in adult animals .It consisted of large columnar cells with dense eosinophilic cytoplasm and large oval basophilic nuclei. These cells showed small, round electron-dense oval granules with variable densities and size. Mitochondria are present but less numerous than that of the fasicuolata cells .It considered adrenaline secreting cells. The inner part of medulla consisted of polyhedral cells, small in size and stained less eosinophilic than the outer cells.It considered nor adrenaline secreting cells. The nor-adrenaline cells contain bigger irregularly shaped electron-dense, oval granules with an intensely electron-dense core.