Monosodium glutamate (MSG) is a widely used food additive, and there is a trepidation that MSG plays a critical role in multiple hepatic disorders. This study was planned to investigate Graviola extract (GE) effects on hepatic and cellular alterations induced by MSG. Fifty Wistar rats were randomly allocated into five groups: control (received normal saline), Graviola (received 200 mg/kg body weight), MSG (received 2.4 gm MSG/kg, 15% of Lethal dose (LD50) of MSG), Graviola + monosodium glutamate (MSG + GE; received GE, 200 mg/kg/day and MSG 2.4 gm/kg body weight (BW) for the next four weeks), and monosodium glutamate + Graviola (received MSG only (2.4 gm/kg BW) daily for four weeks, then concomitant with Graviola (200 mg/kg BW) daily for the next four weeks. MSG and GR were administered orally for eight weeks. Our results showed that MSG caused a significant increase in oxidative stress markers malondialdehyde (MDA), reactive oxygen species (ROS), nitric oxide (NO), hydrogen peroxide (H2O2), proinflammatory cytokines interleukin 6 (IL-6) level, a tumor protein (P53), hepatic cellular damage, as well as proapoptotic markers caspase-3, and B-cell lymphoma 2 (BCL-2)-like protein 4 (Bax). A significant decrease in superoxide dismutase (SOD), catalase (CAT), glutathione S transferase (GST), reduced glutathione (GSH), and an antiapoptotic agent B-cell lymphoma 2 (BCl-2) was observed. The detected MSG effects were normalized by Graviola administration, either a prophylactic or protecting dose. Besides, Graviola reduced the expression of inducible nitric oxide synthase (iNOS) and hepatic fatty acid synthase (FAS) and led to the upregulation of the silent information regulator protein one gene expression gene (SIRT1).In conclusion, the results suggest that Gaviola’s interrelated antiapoptotic, antioxidant, and anti-inflammatory properties are potential mechanisms to enhance hepatic deficits and protect the liver. Graviola can, therefore, be considered a promising hepatoprotective supplement. Additionally, further human clinical trials are also necessary to validate the present research.

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Malathion (MA) is a widely used pesticide in agriculture. It can cause toxicity in different organs of the body. Rosmarinic acid (RO) is found in rosemary extract that can be absorbed through gastrointestinal tract mucosa with potent antioxidant, and anti‐inflammatory potential. The current study is designed to investigate the potential of RO to protect the lung after MA administration. Forty albino rats were allocated equally to four groups. C‐group received corn oil. RO‐group received RO orally. MA‐group received MA. MA‐RO‐group received RO in addition to MA. After three weeks the lungs were dissected for histopathological and biochemical investigations. MA‐group showed manifestations of severe inflammation with inflammatory cells infiltration in the lung. MA‐RO‐group showed limited inflammatory cell infiltration. C‐group and RO‐group appeared with weak anti‐survivin immunoreactivity. MA‐group showed strong positive immunoreactivity. The reactivity was weakly positive in MA‐RO‐group. MA‐group showed a significant decrease in SP‐D gene expression in comparison to the C‐group, in addition, MA‐RO‐group showed a significant increase in SP‐D expression. In conclusion, the current study approves that oral administration of MA causes lung injury as it has inflammatory effects, caused by oxidative stress and reports the potential of RO to protect lung tissue against toxic effects of MA through its anti‐inflammatory, antioxidant, and anti‐apoptotic potential.

Background: Several previous studies explored the toxic effect of high-fat diet (HFD) and high-fructose diet (HFrD), however little is known regarding their differential detrimental effects on the kidney. Aim: This study was conducted to compare the biochemical, histological, and molecular changes in the kidney induced by consumption of HFD and HFrD for 4 and 8 weeks. Materials and Methods: Thirty-five rats were randomly divided into five groups (n = 7/group): control, HFD1 (fed HFD for 4w), HFrD1 (for 4w), HFD2 (for 8w), and HFrD2 (for 8w). The studied parameters involved kidney function markers [urea, creatinine, and retinol-binding protein (RBP)] in the serum, histological examination using H&E stains, immunohistochemical examination of alpha-smooth muscle actin (αSMA), and expression of inflammation and glomerulosclerosis-related genes [tumor necrosis alpha (TNFα), interleukin 1β (IL1β), and nuclear factor kappa B (NFκB)], and necrosis-related genes [poly(ADP-ribose) polymerase-1 (PARP1) and receptor-interacting protein (RIP1)] in the kidney using real-time PCR. Results: Earlier and more severe renal damage were noticed in rats fed HFrD than HFD-fed rats as evidenced by 1) significantly (p<0.05) higher levels of kidney function parameters (urea, creatinine, and RBP), 2) a higher kidney histopathological score (glomerulosclerosis, glomerular necrosis, Bowman's space dilation, coagulative necrosis, cloudy swelling, and fat droplets deposition in renal tubules, congestion and mononuclear cells infiltration in interstitium), 3) a significantly (p<0.01) higher positive αSMA staining in renal capillaries and some tubular cells, 4) a significantly (p<0.05) upregulated expression of (TNFα, IL1β, and NFκB), 5) a significantly (p<0.05) increased expression of (PARP1 and RIP1). The highest damage order was noticed in HFrD2, followed by HFrD1 and then HFD2. No notable renal damage was observed in HFD1 as compared to the control group. Conclusion:The findings of this study highlight the ability of HFrD to induce earlier and more severe renal damage than HFD.

<p><strong>Background:</strong> Cyclophosphamide disturbs the oxidant and antioxidant balance that is associated with several unwanted toxic effects and induction of secondary cancers. The aim of this study was to test the protective effects of Sulforaphane on the cyclophosphamide toxicity of rat urinary bladder.</p><p><strong>Methods:</strong> 32 male albino rats were divided into 4 groups, 8 animal each (n=8). Group I received saline intra-peritoneal, group II received 5 mg/kg sulforaphane for 5 days and then saline, group III received 0.9% saline intra-peritoneal for consecutive 5 days and a single dose of cyclophosphamide 200 mg/kg on the six-day, group IV received sulforaphane at a dose of 5 mg/kg for consecutive 5 days and a single dose of cyclophosphamide 200 mg/kg on the six day. On the seventh day of the experiment, the animals were sacrificed, and the urinary bladder samples were dissected for histopathological and immunohistochemical investigations and electron microscopic studies.</p><p><strong>Results</strong>: the mucosa of the urinary bladder of Sulforaphane treated group showed normal architecture while that of cyclophosphamides treated group showed features of degenerated and ulcerated lesions of the epithelial lining associated with hemorrhage. Theses lesions markedly decreased in the mucosa of urinary bladder of cyclophosphamides and sulforaphane treated group.</p><p><strong>Conclusions</strong>: The use of sulforaphane reduces the cyclophosphamide toxicity on the urinary bladder in the form of decreased vacuolation with decreased degeneration of the epithelial lining.</p>

Introduction: Diet rich in purines may increase the serum level of uric acid causing hyperuricemia contributing learning and memory to impairments. Ascorbic acid has a potent antioxidant potential. The hippocampus is a pivotal component of human brains and other vertebrates that plays crucial roles in the consolidation of information and spatial memory. Our study was mainly designated to examine the potential palliative role of ascorbic acid supplements on harmful effects induced hyperuricemia on the hippocampus of albino Wistar rats. Methods: Forty rats were subgrouped into: Control group, Ascorbate only group, Hyperuricemic group and Combined hyperuricemia and ascorbate group. Results: Ascorbic acid has strongly preserved the histological architecture and maintained the normal hippocampal functions in hyperuricemic group. Discussion/ Conclusion: The anti-inflammatory and antioxidant properties of ascorbic acid could protect the hippocampus of albino Wistar rats against the hazardous impact of hyperuricemia.