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Introduction: Organ phosphorus (OP) toxicity has been studied extensively because of its world wide use. Toxicity of organophosphates is the result of inhibition of acetyl cholinesterase resulting in cholinergic signs. Aim of the Work: To evaluate initial indicators that can indicate prognosis of patients in OP poisoning. Materials and Methods: A retrospective study conducted in Zagazig university hospital over a year. OP poisoning was clinically diagnosed with history of OP compound exposure and confirmed by low pseudo cholinesterase levels. Results: In the present study, 76 patients were enrolled. Major cases were male. High mortality rates were in the youth and in prolonged ventilated patients. The mortality rate was proportionally related to lag time after exposure and plasma pseudo cholinesterase levels. Electrolyte disturbance did not affect clinical outcome. Conclusion: From this study, it could be concluded that mortality is directly proportionate to the lag time, amount of OP consumed, clinical severity, pseudo cholinesterase levels and duration of ventilator support. This study helps in rapid diagnosis, and rapid early and effective treatment, which may result in decreasing the morbidity and mortality rates. Recommendation: It is recommended to increase awareness regarding the rapid diagnosis, and rapid effective treatment of organ phosphorous.

The effect of retinol repletion in previously vitamin A-depleted Lewis rats on antibody production to pneumococcal polysaccharide (SSS-III) was studied. When vitamin A-depleted rats were given either 0.35 mumol (0.1 mg) or 5.2 mumol (1.5 mg) retinol, plasma retinol became normal within 8 h. Liver and lymphoid-organ retinol concentrations were normalized by 1 d after repletion with 5.2 mumol but not 0.35 mumol retinol. Antibody production to SSS-III was compared after administering 5.2 mumol retinol either as a divided dose (half given 4 d before and half given on the day of immunization) or as a single dose concurrent with immunization. Vitamin A-depleted rats produced very little SSS-III-specific antibody. The divided dose of retinol consistently restored anti-SSS-III production whereas the single concurrent dose was less effective despite equal effects on tissue retinol concentrations. Interestingly, normalization of plasma retinol was not always a good predictor of the immune response to pneumococcal polysaccharide.

Tributyltin (TBT) is an organotin compound widely used as a biocide in antifouling paints. Moringa oleifera oil (MOO) has a promising antioxidant potential, which necessitates further exploration. This study was conducted to investigate the potential protective effect of MOO against TBT‐induced brain toxicity. The 30 rats were grouped into five groups (six each), Group I negative control, Group II positive control (vehicle), Group III MOO (5 ml/kg body weight [b.wt.]), Group IV TBT (10 mg/kg b.wt.), and Group V TBT & MOO. All treatments were given orally for 28 days. Thereafter, brains were exposed to oxidative stress and neurological parameters analyses. Histopathological and immunohistochemical (caspase‐3, Bax, Bcl‐2) examinations were also carried out. In rats administered TBT, increased malondialdehyde level, decreased reduced glutathione, and low total antioxidant capacity levels were in support of oxidative stress mechanism. Neurotoxicity was indicated by high nitric oxide level and increased acetylcholinestrase activity. Along with the histopathological alterations, the dysregulated expression of caspase‐3, Bax, and Bcl‐2 were indicative of the apoptotic mechanism mediated by TBT. Co‐administration of MOO with TBT ameliorated the aforementioned toxic effects. In conclusion, TBT causes brain toxicity via oxidative, nitrosative, and apoptotic mechanisms. MOO demonstrates protective effect against TBT‐induced brain toxicity mostly via potent antioxidant and antiapoptotic properties.

Introduction: There are extensive people exposures to paraquat (PQ) herbicide resulting in human health hazards. Aim of the Work: To compare the beneficial neuroprotective effects of hesperidin and benfotiamine on paraquat (PQ)-induced spinal cord neurotoxic effects in rats. Materials and Methods: Rats were divided into 4 groups as following: control, paraquat (PQ 20.8 mg/kg, oral gavage (e.g.)), paraquat + benfotiamine (50 mg/kg, oral gavage (e.g.)) and paraquat + hesperidin (40 mg/kg, oral gavage (e.g.)). PQ is given as the previous dose. Rats are treated 6 days per week. Results: There was a significant increased mean value of malondialdehyde associated with a significant reduction in the content of reduced glutathione and antioxidant enzymes activities associated with a significant increase in Serum phosphorylated neurofilament-H, neurospecific enolase and s100 levels were recorded and significant spinal cord histopathological changes in paraquat treated group as compared to their corresponding values in the control group and immunohistochemical examination confirmed these results. Upon supplementation with benfotiamine and hesperidin to paraquat treated rats, there was a significant decrease in the mean values of malondialdehyde associated with a marked increase in the content of reduced glutathione and antioxidant enzymes activities associated with a significant decrease in Serum phosphorylated neurofilament-H, neurospecific enolase and s100 levels were also recorded with significant improvement of spinal cord architecture when compared with the paraquat treated group. Conclusion: The use of benfotiamine and hesperidin produced a significant protection against all of the above-mentioned changes.

Oxaliplatin is a chemotherapeutic drug used for colorectal cancer treatment. The testicular toxic effect is one of its recorded toxicities which resulted in a few studies. Oxidative stress could be a direct cause of this testicular toxicity. Cerium oxide nanoparticles (CONPs) are optimistic antioxidants for applications in medicine. The aim of the work is to study the protective effect of CONPs on testicular toxicity induced by oxaliplatin in rats. Forty adult male albino rats were divided into 4 groups: Control group, CONPs group (60 mg/kg, 5 times/week), Oxaliplatin group (4 mg/kg, twice/week), and Oxaliplatin & CONPs group, for 4 weeks. Seventy-two hours after the last administration, blood samples were taken for hormonal levels and testes were used for both histopathology and immunohistochemical microscopic examination. Sperm smears were also performed and their results were statistically analyzed to detect any sperm abnormalities. Oxaliplatin increased MDA levels. SOD and GPx activity was decreased. GSH levels were decreased. Also, it decreased the sperm cell count and serum testosterone, and anti-Müllerian hormon. In the testicular sections, significant histopathology changes were seen and immunohistochemical examination confirmed these results. Upon supplementation of CONPs with oxaliplatin decreased MDA levels. SOD and GPx activity was increased, and GSH did not change. In testicular sections, normal morphology was seen. Also, there was an increase in the sperm cell count and serum testosterone anti-Müllerian with significant improvement of testicular architecture, and immunohistochemical examination confirmed these results. The utilization of CONPs produced significant protection against all of the abovementioned changes.

Backgroung: Levo-Carnitine is known L-carnitine that is generally used in medical and nutritional fields. Recent studies highlightened L-carnitine-induced cardiovascular toxic effects. Trimethylamine-N-oxide (TMAO) and heart-type fatty acid-binding protein 3 (HFABP3) are risk markers of its toxicity. Aim of this study was to elucidate the relationship between L-carnitine metabolites and cardiac damage biomarkers in L-carnitine supplemented students. Patients and Methods: This study was carried out on students at tennis section, faculty of physical education for girls, Zagazig University. These students were divided into 2 groups. Group I: Forty nine healthy individuals (age-and grade-matched), and group II: Forty nine L-carnitine supplemented students (1000mg/day in 2 or 3 divided doses orally). Clinical examination and electrocardiography (ECG) were done for all of them. These students have been investigated for L-carnitine, cardiac troponin I (cTn-I), H-FABP3, and TMAO levels. Results: All markers have been significantly elevated when compared with those of the control group. ECG findings were ST depression in 24 students (49%), and T wave inversion in 1 9 students (38.8%) where sinus tachycardia was the commonest finding (77.6%). Furthermore, L-carnitine showed a significant positive correlation with H-FABP3, TMAO, cTn-I, and heart rate. Conclusion: TMAO, HFABP3 seem to be the strongest predictors for long term L-carnitine supplementation's cardiovascular toxicity. Further studies to assess both the efficacy and long term safety of oral L-carnitine supplementation for atheletes that used for physical enhancement were recommended.

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