Lead poisoning has been known as an important disorder that affects individuals through acute, sub-acute and chronic exposure in environmental and occupational settings. This study was conducted to compare the curative role of garlic combined with silymarin versus dimercaptosuccinic acid (DMSA) in decreasing lead induced nephrotoxicity in adult male albino rats. The period of lead intoxication extended for 3 months followed by either 1 month treatment with garlic and silymarin or 5 days treatment with DMSA. Lead poisoning caused non-significant difference in kidney function tests (BUN and serum creatinine) while, it caused significant elevation in kidney lead level, significant decrease in renal antioxidant enzyme glutathione peroxidase and significant elevation in kidney malondialdehyde. Histologically, lead induced disorganization and shrinkage of glomeruli with sloughing and vaculation of epithelium, widening of Bowman's space and inflammatory infiltration in renal medulla. Treatment by garlic extract combined with silymarin as well as treatment with DMSA resulted in significant improvement in the affected parameters. Also, both methods of treatment resulted in improvement of the histopathological changes. It can be concluded that garlic extract combined to silymarin is comparable to DMSA in amelioration of lead induced nephrotoxicity.
Lead (Pb) is one of the most common toxic heavy metals. It is a well-known testicular toxicant. Selenium nanoparticles (SeNPs) are a more effective form of elemental selenium that reduces drug-induced toxicities. This study aimed to study the possible ameliorating effect of SeNPs on the toxicological and morphological changes in testes of lead acetate intoxicated rats. The study was conducted on 40 adult male albino rats divided into four groups; control, SeNPs-treated, lead acetate-treated, lead acetate and SeNPS treated groups.The concurrent treatment of lead acetate-exposed rats with SeNPs (0.1 mg/kg/ day) for 12 weeks significantly lowered the blood and testicular lead levels, increased serum testosterone, and decreased luteinizing hormone and folliclestimulating hormone to approach control values. In addition, it improved the histopathological, and ultrastructural alterations of the testes and improved the immunohistochemical expression of the c-kit. This was accompanied by maintenance of the testicular oxidant/antioxidant balance and reversing the lead-induced disrupted calmodulin-related genes expression in testicular tissue in the form of downregulation of CAMMK2 and MAP2K6 and upregulation of CXCR4 genes. There was a strong positive correlation between testicular malondialdehyde and MAP2K6 expression level as well as a strong positive correlation between CXCR4 gene expression and the C-kit area %. In conclusion, SeNPs can be considered as a potential therapy for a lead-induced testicular injury.
This study was designed to investigate structural and ultra-structural changes induced by nitrate in rat liver, examine their molecular basis, and evaluate the possible protective role of S-Allylcysteine (SAC). Adult male albino rats were assigned to: control, SAC, nitrate, and nitrate+ SAC groups. Serum ALT and AST were measured. Liver samples were processed for light and electron microscope examinations, biochemical analysis, real-time PCR, and immunohistochemistry of heat shock protein 70 (HSP70) and Bcl-2. Nitrate induced histopathological and biochemical alterations in rat liver. The underlying mechanisms included nitrosative and oxidative stress, inflammation, fibrosis, and apoptosis that are alleviated by SAC.
Toluene was widely used volatile organic compound that accumulates in tissues with high lipid content. Stem cells have been proposed as an increasingly attractive approach for repair of damaged nervous system, we aimed to evaluate the ability of breast milk mesenchymal stem cells (MSc) to ameliorate toluene-induced encephalopathy. Sixty adult male albino rats were assigned to 3 groups, control, toluene, and toluene/breast milk-MSc. Neurological assessment was evaluated as well as serum levels of glial fibrillary acidic protein (GFAP), tumor necrosis factor-alpha (TNF-α), nerve growth factor (NGF), vascular endothelial growth factor (VEGF), tissue dopamine and oxidative markers. Gene expression of peroxisome Proliferator-Activated Receptor-Gamma (PPAR-ɣ), nuclear factor-kappaB (NF-kB), and interleukin-6 (IL-6) were evaluated. Moreover, histological and immunohistochemical investigation were done. Results revealed that toluene caused cerebral injury, as evidenced by a significant increase in serum GFAP, TNF-α, malondialdehyde (MDA) and nitric oxide (NO), a significant decrease in serum NGF, tissue dopamine and oxidative markers, besides, a non-significant change in VEGF. Toluene also caused changes in normal cerebral structure and cellular degeneration, including a significant decrease in the total number of neurons and thickness of frontal cortex. Meninges showing signs of inflammation with inflammatory cell infiltration and exudation, a significant decrease in MBP immunoreactivity, and increase in the percent of high motility group box protein-1 (HMGB1) positive cells. PPAR- ɣ, NF-kB, and IL-6 gene expression were all considerably elevated by toluene. These changes were greatly improved by breast milk MSc. Therefore, we conclude that breast milk MSc can attenuate toluene-induced encephalopathy.
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