Yasser S. El-Sayed

Acute intoxication of deltamethrin in monosex Nile tilapia, Oreochromis niloticus with special reference to the clinical, biochemical and haematological effects.

Deltamethrin, a synthetic pyrethroid pesticide, potential toxic pollutant and significant direct risk to the aquatic ecosystems, was investigated in the present study for its toxic impact on adult monosex Nile tilapia on the basis of acute static bioassay test, and comparison of clinical, biochemical and haemato logical examinations with deltamethrin-free control group. The 96hLC(50) value of deltamethrin for monosex tilapia was 14.6μg/L. The abnormal behavioral responses and toxic symptoms were described. Fish exposed to the higher deltamethrin concentration (15μg/L) for 96h showed significantly higher lymphocytes, total leucocytic and erythrocytic counts, haemoglobin percentage and packed cell volume content and significantly lower neutrophils compared to the control group. Deltamethrin caused adverse effects in the form of hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypoglycemia and significant increase of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities. The results provide evidence that deltamethrin pollution may have adverse impacts and was highly toxic to monosex tilapia.

Oxidative stress and immunotoxic effects of lead and their amelioration with myrrh (Commiphora molmol) emulsion.

The possible role of Commiphora molmol emulsion (CME) in protecting against lead (PbAc)-induced hepatotoxicity, oxidative stress and immunotoxicity in rabbits was assessed. Six groups of animals were used: groups I (control) and II (PbAc) were not supplemented with CME. Groups III (CME50) and IV (CME50+PbAc) were administered with CME in a dose rate of 50mg/kg bwt, while groups V (CME100) and VI (CME100+PbAc) were received 100mg CME/kg bwt daily p.o for successive 14 weeks. Groups II, IV and VI were given 80 mg PbAc/kg bwt/day orally for 6 weeks starting from the 9th week. At the 12th week, animals were subjected to immunization by a single dose of sheep RBCs. The PbAc-group showed 220% increase in hepatic malondialdehyde levels, while glutathione, glutathione s-transferase and glutathione peroxidase levels decreased. Lead-acetate induced hypoproteinemia and hypoalbuminemia, and increased aminotransferases activity. It reduced the values of lymphocyte transformation test, phagocytic activity, phagocytic index and antibody titer against sheep SRBCs. Interestingly, pretreatment with CME attenuated these adverse effects in a dose-dependent protection. CME, therefore, is a potent antioxidant, and can protect against PbAc-induced hepatic oxidative damage and immunotoxicity by reducing lipid peroxidation and enhancing the antioxidant and immune defense mechanisms.

Influence of vitamin C supplementation on lead-induced histopathological alterations in male rats.

This study is intended to evaluate the efficacy of vitamin C (VC) in ameliorating the detrimental effects of long-term lead intoxication on the liver, kidneys, brain and testes as assessed by histopathology. A total of forty male Wistar rats (six-weeks-old) was divided into 4 groups: control group; lead-acetate (PbAc)-treated group (20 mgPbAc/kgbwt); PbAc+VC-treated group (20 mgPbAc/kgbwt plus 20 mg VC/kgbwt); and VC-treated group (20 mgVC/kgbwt). The Experimental period was lasted for 60 successive days in which PbAc was administered once daily while VC was supplemented every other day using intra-gastric intubation. At the end of the experimental period, all rats were sacrificed and pathological examinations were performed. Control and VC-supplemented rats showed normal liver, kidney, brain, and testes histology. In contrast, the liver of PbAc-intoxicated rats exhibited degenerated hepatocytes and portal inflammatory cell infiltrations. The kidneys showed degenerated glomeruli and formation of karyomegalic cells containing intranuclear inclusions in the proximal tubular epithelium. Cerebellar edema, cerebral satellitosis and encephalomalacia observed in the brain. Testicular tissues showed arrest of spermatogenesis and interstitial edema. Co-administration of VC with PbAc diminished the severity of pathological changes and reduced the number of affected organs compared to PbAc-intoxicated rats. These results show that low level of VC ameliorated and mitigated the adverse pathological impacts of chronic lead toxicity.

Toxicity, biochemical effects and residue of aflatoxin B1 in marine water-reared sea bass (Dicentrarchus labrax L.)

Aflatoxicosis and resulting epizootic hepatoma have been reported among a wide range of fish where Aspergillus species-contaminated foodstuffs are incorporated into the diet. Aflatoxin B(1) (AFB(1)) is among the most potent known hepatotoxins and carcinogens. Therefore, it is an important potential toxicant to the most of the popularly cultured fish species. The present study was undertaken to assess the susceptibility and toxicity of AFB(1) to sea bass (Dicentrarchus labrax L.), by behavioral and biochemical evaluations. The estimated oral acute median lethal concentration (96 h LC(50)) of AFB(1) for sea bass was 0.18 mg/kg bwt. The abnormal behavioral responses and signs of toxicity were described. The prolonged oral administration of 0.018 mg/kg bwt AFB(1) to sea bass for 42 successive days induced a significant increase in serum transaminases and alkaline phosphatase activities, and significant decrease in plasma proteins. Residual AFB(1) was detected at high levels ( approximately 5 ppb) in fish musculature at the end of the experimental period. We conclude that marine water sea bass is a species highly sensitive to AFB(1). In addition, consumption of sea bass reared on AFB(1)-contaminated diet could have a negative health impact on human health.

Chicory (Cichorium intybus L.) Root Extract Regulates the Oxidative Status and Antioxidant Gene Transcripts in CCl4-Induced Hepatotoxicity

The ability of Cichorium intybus root extract (chicory extract) to protect against carbon tetrachloride (CCl4)-induced oxidative stress and hepatotoxicity was evaluated in male rats. The rats were divided into four groups according to treatment: saline (control); chicory extract (100 mg/kg body weight daily, given orally for 2 weeks); CCl4 (1 ml/kg body weight by intraperitoneal injection for 2 consecutive days only); or chicory extract (100 mg/kg body weight daily for 2 weeks) + CCl4 injection on days 16 and 17. The levels of hepatic lipid peroxidation, antioxidants, and molecular biomarkers were estimated twenty-four hours after the last CCl4 injection. Pretreatment with chicory extract significantly reduced CCl4-induced elevation of malondialdehyde levels and nearly normalized levels of glutathione and activity of glutathione S-transferase, glutathione peroxidase (GPx), glutathione reductase, catalase (CAT), paraoxonase-1 (PON1), and arylesterase in the liver. Chicory extract also attenuated CCl4-induced downregulation of hepatic mRNA expression levels of GPx1, CAT and PON1 genes. Results of DNA fragmentation support the ability of chicory extract to ameliorate CCl4-induced liver toxicity. Taken together, our results demonstrate that chicory extract is rich in natural antioxidants and able to attenuate CCl4-induced hepatocellular injury, likely by scavenging reactive free radicals, boosting the endogenous antioxidant defense system, and overexpressing genes encoding antioxidant enzymes.

Carbon black nanoparticle exposure during middle and late fetal development induces immune activation in male offspring mice

Increasing exposure to nanoparticles (NPs) has raised concerns regarding their health and safety profiles in humans and animals, especially in developing organisms, which may display increased sensitivity to NP toxicity. The present study examined the effects of gestational exposure to carbon black NP (CB-NP) on the development of the offspring immune system. Pregnant mice were exposed to CB-NP (95μg/kg body weight) by intranasal instillation on gestational days 9 and 15. The thymus and spleen were collected from their offspring mice on postnatal day (PND) 1, 3 and 5. Thymocyte and splenocyte phenotypes were examined by determining the expression of cell-surface molecules using flow cytometry. Gene expression in the thymus and spleen was examined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Prenatal exposure to CB-NP increased total thymocytes and their immunophenotypes (CD4(-)CD8(-) and CD4(+)CD8(+) cells). It also induced an increase in total lymphocytes, and CD4(-)CD8(-), particularly CD3(-)B220(-)cells, at PND 5 in the spleen of newborn male offspring, reflecting the stimulation of immature splenocytes. Furthermore, mRNA expression of genes related to the induction of peripheral tolerance (i.e. thymic Traf6) was upregulated. These data suggest that respiratory exposure to CB-NP during middle and late gestation may have allergic or inflammatory effects in male offspring, and may provide initial information on the potential developmental immunotoxicity of nanoparticles.

Therapeutic effects of date palm (Phoenix dactylifera L.) pollen extract on cadmium‐induced testicular toxicity

Cadmium (Cd) is a well‐known testicular toxicant. This study was designed to explore the long‐term effects of a single low dose of Cd on spermatogenesis, and testicular dysfunction and oxidative stress, and the therapeutic potential of date palm pollen extract (DPP) in averting such reproductive damage. Adult male Wistar rats received a single intraperitoneal injection of CdCl2 (0 or 1 mg kg−1). Twenty‐four hours later, they started receiving DPP (0 or 40 mg kg−1) orally, once daily for 56 consecutive days. Cd exposure caused significant reproductive damage via reduced weight of the reproductive organs, which includes spermatological damage (decreased sperm count and motility and increased rates of sperm abnormalities), increased oxidative stress (increased malondialdehyde and decreased reduced glutathione levels), histological alterations (necrosis, inefficient to completely arrest spermatogenesis and a reduced Johnsens score) and decreased serum testosterone level. DPP restored spermatogenesis and attenuated the toxic effects of Cd on the reproductive system to the levels observed in the control animals. These findings support the hypothesis that the testis is particularly sensitive to Cd, which can cause testicular damage and infertility. Treatment with DPP can ameliorate the deleterious effects of Cd, probably by activating testicular endocrine and antioxidant systems.

Synergistic ameliorative effects of sesame oil and alpha-lipoic acid against subacute diazinon toxicity in rats: hematological, biochemical, and antioxidant studies.

Diazinon (DZN) is a common organophosphorus insecticide extensively used for agriculture and veterinary purposes. DZN toxicity is not limited to insects; it also induces harmful effects in mammals and birds. Our experiment evaluated the protective and antioxidant potential of sesame oil (SO) and (or) alpha-lipoic acid (ALA) against DZN toxicity in male Wistar albino rats. DZN-treated animals exhibited macrocytic hypochromic anemia and significant increases in serum biochemical parameters related to liver injury, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), γ-glutamyl transferase (γGT), cholesterol, and triglycerides. They also had elevated levels of markers related to cardiac injury, such as lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), and increased biomarkers of renal injury, urea and creatinine. DZN also increased hepatic, renal, and cardiac lipid peroxidation and decreased antioxidant biomarker levels. SO and (or) ALA supplementation ameliorated the deleterious effects of DZN intoxication. Treatment improved hematology and serum parameters, enhanced endogenous antioxidant status, and reduced lipid peroxidation. Importantly, they exerted synergistic hepatoprotective, nephroprotective, and cardioprotective effects. Our findings demonstrate that SO and (or) ALA supplementation can alleviate the toxic effects of DZN via their potent antioxidant and free radical-scavenging activities.

Acute toxicity of ochratoxin-A in marine water-reared sea bass (Dicentrarchus labrax L.)

The toxic effects of ochratoxin-A (OTA) on sea bass, Dicentrarchus labrax L., have not been previously documented. A flow-through bioassay test system was conducted in two series and a total 180 of adult marine-reared sea bass was used to estimate the acute oral 96 h median lethal concentration (LC(50)) value and behavioral changes of OTA. The data obtained were statistically evaluated using Finneys Probit Analysis Method developed by EPA. The 96 h LC(50) value for adult D. labrax was found to be 277 microg kg(-1)bwt with 95% confidence limits of 244-311 microg kg(-1)bwt. This value was calculated to be 285 microg kg(-1) bwt with Behrens-Karbers method. The two methods were relatively comparable. The acute dietary 96 h LC(50) of OTA is 9.23 mg kg(-1) diet. Additionally, the behavioral changes of sea bass were primarily observed as nervous and respiratory manifestations. We concluded that sea bass is a species highly sensitive to OTA making them a useful experimental model for aquatic mycotoxigenic problems.

Ginger extract modulates Pb-induced hepatic oxidative stress and expression of antioxidant gene transcripts in rat liver

Abstract Context: Spices and herbs are recognized sources of natural antioxidants that can protect from oxidative stress, thus play an important role in chemoprevention of liver diseases. Ginger is used worldwide primarily as a spicy condiment. Objective: This study evaluated the ability of ginger extract (GE) to ameliorate oxidative-hepatic toxicity induced by lead acetate (PbAc) in rats. Materials and methods: Five groups of animals were used: group I kept as control; groups II, IV, and V received PbAc (1 ppm in drinking water daily for 6 weeks, and kept for an additional 2 weeks without PbAc exposure); group III treated orally with GE (350 mg/kg body weight, 4 d per week) for 6 weeks; group IV (protective) received GE for 2 weeks before and simultaneously with PbAc; and group V (treatment) received GE for 2 weeks after PbAc exposure. Results: GC-MS analysis of GE revealed its content of gingerol (7.09%), quercetin (3.20%), dl-limonene (0.96%), and zingiberene (0.18%). Treatment of PbAc-treated rats with GE has no effect on hepatic Pb concentrations. However, it maintained serum aspartate aminotransferase level, increased hepatic glutathione (157%), glutathione S-transferase (GST) (228%), glutathione peroxidase (GPx) (138%) and catalase (CAT) (112%) levels, and reduced hepatic malondialdehyde (80%). Co-treatment of PbAc group with GE upregulated mRNA expression of antioxidant genes: GST-α1 (1.4-fold), GPx1 (1.8-fold), and CAT (8-fold), while post-treatment with GE upregulated only mRNA expression of GPx1 (1.5-fold). Conclusion: GE has an antioxidant protective efficacy against PbAc-induced hepatotoxicity, which appears more effective than its therapeutic application. However, the changes in antioxidant gene expression were not reflected at the protein level.