[en] The buthus occitanus, scorpion venom contains a strong bradykinin potentiating factor (BPF) that augments bradykinin effects through enhancing its release. Based on the cytoprotective ability of BPF, the present work investigates it as a radioprotectant. Sublethal whole-body y-irradiation at 1.5 Gy was used. Bone marrow cells suspension (BM cells) alone or in combination with BPF was utilized. Three to four weeks-aged male Guinea pigs were grouped into two major groups. The first was non-irradiated control that was divided into subgroups treated ip with BM cells (2.5 xl06 cells), one dose of BPF (lug/gb wt), BM cells+ BPF, one week spaced two doses of BPF, BM cells+ 2 doses of BPF, one week spaced three doses of BPF or BM cells+ 3 doses of BPF. Second major group (irradiated group) at 1.5 Gy that, subdivided and treated similarly. 5 animals from each group were killed at 7, 14 and 21 days from the initiation of treatment (3 h after irradiation). The subgroups of non-irradiated animals showed an increase in spleen wt and colony formation, thymus population, and globulins content particularly in those subgroups that stayed for the later time periods (14 and 21 days) and that treated with combined BM cells+ BPF or that groups that were treated with two or three BPF doses. Irradiation caused dramatic destruction in thymus and the spleen reflected on reduction of the lower globulins content. Treatment with BM cells, BM cells+ double doses of BPF or triple doses of BPF caused complete recovery in all measured indices, the best result was observed in those of subgroups treated with BM cells+ double doses of BPF or treated with triple …

ABSTRACT
Cisplatin (CP) is considered as a major antineoplastic drug against a broad spectrum of malignancies. CP acts on cancer cells by releasing free radicals which at the same time damage liver and kidney cells. The tissue specific toxicity of cisplatin to the kidneys is well documented. However, at higher doses less common toxic effects such as hepatotoxicity may arise. Strategies to protect tissues against CP toxicity are of clinical interest. In this study, we aimed to investigate the hepatotoxicity of CP which it may be mediated by oxidative stress and to establish whether some antioxidants, namely vitamin C, N,NDiphenyl- X-phenylenediamine (DPPD) and L-cystiene, may provide protection against CP hepatotoxicity. Forty adult male albino rats (1 20-1 50 g) were divided into 5 groups (8 rats each). CP was injected once a week (2 mg/kg) for four weeks. The antioxidants DPPD (1 25 mg/kg b.w. ), vitamin C (1 00 mg/kg) and L-cystiene (1 00 mg/kg) were also injected once a week 24 hour prior to CP injection. The control group
was injected with saline. All doses were injected intraperitoneally. Rats of different groups were killed by cervical dislocation, 24 hours after the last injection and blood was collected into a sterilized tube containing EDTA to separate plasma. The livers was taken for histological and biochemical examinations. CP-induced oxidative stress was indicated by increased level of LPO and superoxide anion in hepatic tissue and plasma. Also, CP induced decline of antioxidant enzymes such as SOD, CAT, GST and GGT and a decreased level of GSH, Vit. C and Vit. E in hepatic tissue and plasma. Treatment with Vit. C, DPPD and L-cysteine in combination with CP restored LPO and superoxide anion,
the activities of SOD, GST, CAT and GGT and the content of GSH, Vit. C and Vit. E to about normal control levels. in conclusion treatment with Vit. C, DPPD or L-cysteine in combination with CP may be effective to protect from oxidative hepatic injury that induced by CP treatment.

The present study was planned to investigate the effect of dietary supplementation with copper Chelating complex as immunstimulant of catfish Claris gariepinus. Forty acclimated African sharp tooth catfish, were divided into two groups. The first group (control group G I) received the basic diet, for 30 days. The second group received the basal diet mixed with 60 mg copper albumin chelating complex/kg basal diet; (G II). At the end of 30 days feeding, the fish of each group were, weight, blood film and serum sample were collected and tested. Fish of each group were challenged by local strain of Aeromonas hydrophila, for challenge. The clinical signs, P.M. lesions and mortalities were also monitored for 7 days post challenge. The obtained results were indicated that copper chelating complex improve the growth rate, and enhance the protective effect against challenge with A. hydrophila and potentiate the non-specific immune response through increase the percent of basophile, the lymphocytes and increase the total protein and the globulin in the blood of the treated fish. In conclusion use of copper chelating complex as feed additive for Clariasgariepinus at a dose of 60mg / kg diet has shown to be an activator of non-specificimmune response.

In a previous work we have reported that synthetic copper (I)-nicotinate complex efficiently prevented induced nephrotoxicity by Aflatoxin B1 (AFB1) specifically by promoting phase II detoxificating glutathioneS-transferase activity. This work has been conducted to evaluate the antitoxic effect of the complex on the metabolism of AFB1. Forty five healthy male Wister albino rats were intoxicated (20 µg/kg B.W.) day after day for five weeks. The individually collected urine was assayed for AFB1, AFM1 and AFQ1 contents by HPLC technique. One third of them were co-treated by butylated hdroxytoluene (BHT) (0.05 g/kg B.W.), the second was co-treated by the copper complex (400 µg/kg B.W.) while the last was only intoxicated untreated group. Significant increase in the less toxic AFM1 and AFQ1 metabolites was recorded by any of the co-treating agents. The output of the least toxic AFQ1 fraction was significantly increased by the copper complex as regard to the BHT, (P <0.05). Conclusively, AFM1 and AFQ1 fractions in the urine that were promoted by the two tested agents may be related to their potentiating activity upon the phase I detoxificating CYP 1A2 and 3A4 enzyme families respectively. The significantly increased detoxified AFQ1 metabolite may be preferentially promoted by the copper (I)-nicotinate complex. This beneficial detoxificating effect of the copper complex has been obviously confirmed by observed great reduction in the immunohistochemical detection of vascular endothelial growth factor that was highly initiated by aflatoxicosis. Hence, such a complex could be saftly accepted as a highly potent antitoxic agent against aflatoxicosis

This submitted work was designed in order to evaluate the prophylactive efficacy of the synthetic copper (I)-nicotinate complex against nephrotoxicity by aflatoxin B1 (AFB1) with regard to the highly accepted antioxidant agent butylated hydroxytoluene (BHT). Aflatoxin B1 fraction was obtained by growing Aspergillus flavus in potato dextrose agar (PDB) liquid medium. Healthy young males albino rats (n= 45) were exposed to AFB1 day after day for five weeks (20 µg/kg body weight). One third of them was co-treated with BHT (0.05 g/kg body weight) and the second third by the copper complex (400 µg/kg body weight) while the third was considered as only intoxicated control group. Such intoxication resulted into the histopathological (light and electron transmission) characteristic features of nephrotoxicity. The sever degenerative changes swelling of the cells even rapture of the membrane and cellular organelles in the tubular lumen as well as fibrocytic reaction and congestion of the vasculature in addition to glomerular reaction manifested by atrophy of both vesiral (bodocyte) and parital shirnked cells. The co-treated BHT group did not eliminate all such features of degenerative characters in intoxicated tissue kidney while the co-treated copper complex group mostly appeared normal. The enzyme level of phase II of body detoxificating GST was significantly increased than that improved by BHT. Conclusively, the food additive probable use of the copper nicotinate complex could be a promising agent against nephrotoxicosis.

Hepatitis C virus (HCV) infection represents a world health problem and no protective vaccine or effective drug currently exists. For economic reasons, many patients use traditional medicines to control the infection. In Egypt, camel milk is one of the traditional medicines widely consumed by patients infected with HCV. The present study aimed to evaluate the efficacy of camel milk in the treatment of patients infected with HCV. Whole camel milk from a local farm was administered to patients for 4 months (250 ml/day/patient). Patient sera were collected prior to and following camel milk drinking, and three markers were set‑up for sera‑evaluation. The three markers indicating the effect of camel milk on HCV infection were: Liver function assays [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)]; a viral load assay; and anti‑HCV antibodies profile and isotyping against synthetic HCV epitopes. Camel …

This study was performed to examine that copper-albumin complex can restore oxidative damage and cytotoxicity in induced by Bromobenzene (BB) in liver. Rats were divided into three groups. Group I served as control received corn oil only. Group II exposed to BB at a dose of 300 mg/Kg by weight, twice/week, orally, dissolved in corn oil for one month. Group III received BB as previous dose plus copper albumin- Serum total protein and albumin showed significant reduction while the activities of ALT and AST enzymes significantly increased in BB-treated group when compared to control. The antioxidant enzymes activities were found to be decreased in BB treated rats in contrast nitric oxide and lipid peroxidation levels were increased in comparison with normal control. Histopathology revealed that BB had a hepatotoxic effects represented by hepatitis and fatty degeneration. Nile blue positive stain showed lipofuscin and/or ceroid granules. Necrotic nuclei with disintegrated DNA stained with acridine orange. The treated rats with copper-albumin complex reversed the most of parameters to normal control.

ABSTRACT

Background: Abnormal plasma levels of free amino acids may predict the severity in patients with drug resistant epilepsy (PRE), having probability to affect their therapeutic approach.

Objectives:We aimed to illuminate the effect of plasma free amino acids (PFAAs) profiles on the etiology of patients with PRE and their contribution on the frequencies of epileptic fits.

Patients and Methods:We collected clinical and metabolomic data of 90 subjects; 45 of them were PRE patients, and other 45 age and sex matched healthy controls. Quantitative measurements of PFAAs profiles using SykamAutomatic Amino Acid Analyzer S433, in addition to fasting blood sugar, liver function tests, kidney function tests and lipid profile also, were determined.

Results: The plasma levels of glutamate, glycine and Gamma amino butyric acid(GABA) plasma levels were significantly increased in PRE group compared to controls (p˂0.0001),their plasma levels also showed significant increase with increased frequency of epileptic fits. Plasma leucine, phenylalanine, aspartate ,ornithine, citrulline, serine and alanine levels (p˂0.0001) were significantly increased in PRE group in relation to healthy controls. Interestingly, on the other hand, histidine, isoleucine, lysine, threonine and the amino acid derivative taurine levels were significantly decreased in PRE patients compared to healthy controls.

Conclusion:Few biomarkers of PRE are available to find the severity and rate of progressionof PRE. The present study showed that altered plasma amino acids and their derivatives may be candidate markers for PRE, help explaining its pathogenesis, and for further researches concerning normalization of the disturbed amino acid/s or its derivative/s (GABA and taurine) in managing PRE patients.

Keywords:Aminogram; Plasma free amino acid profile; Pharmacoresistant epilepsy, amino acids. Abbreviations:Anti-epileptic drugs (AEDs), Branched-chain amino acids (BCAAs), Plasma free amino acids (PFAAs),Pharmaco-resistant epilepsy (PRE).