Hepatic damage associated with fatal zinc phosphide poisoning in broiler chicks

AbstractZinc phosphide (Zn3P2) is a widely used rodenticide which has the potential to cause high mortality if ingested. The present study was designed in order to explore the hepatic injury in broiler chicks that were acutely intoxicated with Zn3P2. For this purpose, a total number of 12 broiler Saso chicks were divided into two equal groups. Birds of the first group were exposed to 300ppm Zn3P2 via food. Hepatic damage of intoxicated birds was evaluated biochemically and histologically using the transmission electron microscope and subsequently compared with another healthy non-treated controls (second group). The serum activity of aspartate aminotransferase (AST) was significantly higher in those poisoned with Zn3P2, While, activities of both Alanine aminotransferase (ALT) and Alkaline phosphatase (ALP), as well as, zinc concentration of hepatic tissue did not represented a significant difference between treated and control birds. Histological examination revealed presence of numerous heterogenic shaped mitochondria in hepatocytes of non-treated birds. Glycogen deposits were also scattered in the form of large electron dense deposits. Kupffer cell was irregular in shape and had numerous pseudopods often projected into sinusoidal lumen. In hepatic cells of intoxicated birds, mitochondrial swelling with cristolysis, few glycogen deposits, vacuoles in the cytoplasm and shrunken darkly stained nuclei are the major ultra-structural changes which were detected. It was concluded that the mitochondria could be one of the main target in hepatocytes for the toxic effect of Zn3P2 in broiler chicks

Evaluation of acute toxicity of genabilic acid (menbutone 10%) in rabbits

[EN] A complete investigation of the acute toxicity of a choleretic compound, menbutone, was performed in rabbits, including lethal dose for 50% of rabbits determination, clinical signs observation and in vivo and post-mortem examinations. Haematological, biochemical and histopathological changes resulting from intramuscular injection of menbutone were also investigated at dose 400 mg/kg body weight. Acute toxicity of menbutone at dose of 400 mg/kg BW induced interstitial myocarditis and multifocal necrosis, whereas serum creatine phosphokinase, creatinine phosphokinase-MB isoenzyme and aspartate aminotransferase activities were significantly increased. Elevation of serum alanine aminotransferase and alkaline phosphatase activities and total bilirubin level associated with lowered albumin content was consistent with histopathological changes of hepatic tissues; hepatic necrosis and fatty infiltration were pronounced indicators of injuries. Renal tubular necrosis and interstitial nephritis were also observed in intoxicated rabbits. Menbutone also induced variations in some haematological parameters. We concluded that acute toxicity of menbutone in rabbits occurred at accidental high doses, as the lethal dose was about 50 fold over the recommended therapeutic dose for other animals. Cardiac muscle, liver and kidneys are the main target organs for menbutone toxicity. Menbutone is not recommended for use in rabbits suffering from any cardiacand hepatic disorders, especially in overdosing situations.El Okle, SO.; Tohamy, GH.; Lebda, AM. (2014). Evaluation of acute toxicity of genabilic acid (menbutone 10%) in rabbits. World Rabbit Science. 22(3):215-222. doi:10.4995/wrs.2014.1791.SWORD215222223Cardinale, D., Sandri, M. T., Colombo, A., Colombo, N., Boeri, M., Lamantia, G., … Cipolla, C. M. (2004). Prognostic Value of Troponin I in Cardiac Risk Stratification of Cancer Patients Undergoing High-Dose Chemotherapy. Circulation, 109(22), 2749-2754. doi:10.1161/01.cir.0000130926.51766.ccCulling C.F. 1983. Handbook of Histopathological and Histochemical Techniques, 3rd ed. London, Boston: Butterworth.De la Cruz-Hernández N.I., Argudín-Salomón O.A., Zertuche- Rodríguez J.L., Medellín-Ledezma J.A., Flores-Gutiérrez G.H. 2012. Case report: outbreak of sodium monensin intoxication in feedlot cattle from Mexico. Revue Med. Vet., 163: 60-63.Pershin G.N. 1971. Methods of experimental chemotherapy: Practical guidance, 2nd edition, Moscow. Russia: Medicina

Histological, ultrastructural, and genetic investigatory comparison between different types of experimentally - Induced antemortem burns

Background: Burn is a cutaneous injury that is caused by heat, electricity, chemicals, freezing, and radiation. Aims and Objectives: This study aimed to differentiate between dry heat burn injury and other common cutaneous burn injuries. Materials and Methods: For this, different types of dermal burns were created experimentally in four groups of rats, 5 rats for each, as the following: dry heat burn model, scalding model, chemical burn model, and electrical burn model. The burnt skin and hair samples were subjected to scanning electron microscopic examination, molecular assay of aquaporin-3 (AQP-3) gene expression, and histopathological investigation. Results: There were crakes, holes, and cuticular irregularity in hairs exposed to both dry heat and sulfuric acid (chemical burn), while the major lesion observed in hairs exposed to boiling water (scald injury) was cuticular cell loss. On the other hand, dry burnt skin showed empty orifices of the hair and sebaceous gland with overlapped smooth lamella, while scald induced irregularity of collagen fibers. The sulfuric acid produces separation of the epidermis from the dermis and irregularity in collagen fiber. Rat skin exposed to electric current appears with fissure, lacerated edges, and erected broken hairs. Despite AQP-3 gene expression was significantly upregulated in the burnt skin of all experimental models in comparing with control rats, dry heat burned skin showed the highest upregulated level. In addition, the coagulation of the dermoepidermal cells and vesicles formation were the most pronounced lesions observed in all types of burns, while scald was distinguished by appearance of elongated cellular nuclei. Conclusion: These observations suggest the possibility to differentiate between dry thermal burn, scald injury, chemical burn, and electrical burn using the combination between scanning electron microscopic examination, analysis of cutaneous AQP-3 gene expression, and histological investigation

Ornipural^® Mitigates Malathion-Induced Hepato-Renal Damage in Rats via Amelioration of Oxidative Stress Biomarkers, Restoration of Antioxidant Activity, and Attenuation of Inflammatory Response

The current study was instigated by investigating the ameliorative potential of Ornipural® solution against the hepato-renal toxicity of malathion. A total number of 35 male Wistar albino rats were divided equally into five groups. Group 1 served as control and received normal saline intraperitoneally. Group 2, the sham group, were administered only corn oil (vehicle of malathion) orally. Group 3 was orally intoxicated by malathion in corn oil at a dose of 135 mg/kg BW via intra-gastric gavage. Group 4 received malathion orally concomitantly with Ornipural® intraperitoneally. Group 5 was given Ornipural® solution in saline via intraperitoneal injection at a dose of (1 mL/kg BW). Animals received the treatment regime for 30 days. Histopathological examination revealed the harmful effect of malathion on hepatic and renal tissue. The results showed that malathion induced a significant decrease in body weight and marked elevation in the activity of liver enzymes, LDH, and ACP. In contrast, the activity of AchE and Paraoxonase was markedly decreased. Moreover, there was a significant increase in the serum content of bilirubin, cholesterol, and kidney injury markers. A significant elevation in malondialdehyde, nitric oxide (nitrite), and 8-hydroxy-2-deoxyguanosine was observed, along with a substantial reduction in antioxidant activity. Furthermore, malathion increased tumor necrosis factor-alpha, the upregulation of IL-1B, BAX, and IFN-β genes, and the downregulation of Nrf2, Bcl2, and HO-1 genes. Concurrent administration of Ornipural® with malathion attenuated the detrimental impact of malathion through ameliorating metabolic biomarkers, restoring antioxidant activity, reducing the inflammatory response, and improving pathologic microscopic alterations. It could be concluded that Ornipural® solution demonstrates hepatorenal defensive impacts against malathion toxicity at biochemical, antioxidants, molecular, and cellular levels

Ginseng^® Alleviates Malathion-Induced Hepatorenal Injury through Modulation of the Biochemical, Antioxidant, Anti-Apoptotic, and Anti-Inflammatory Markers in Male Rats

This study aims to see if Ginseng® can reduce the hepatorenal damage caused by malathion. Four groups of forty male Wistar albino rats were alienated. Group 1 was a control group that got orally supplied corn oil (vehicle). Group 2 was intoxicated by malathion dissolved in corn oil orally at 135 mg/kg/day. Group 3 orally received both malathion + Panax Ginseng® (300 mg/kg/day). Group 4 was orally given Panax Ginseng® at a 300 mg/kg/day dose. Treatments were administered daily and continued for up to 30 consecutive days. Malathion’s toxic effect on both hepatic and renal tissues was revealed by a considerable loss in body weight and biochemically by a marked increase in liver enzymes, LDH, ACP, cholesterol, and functional renal markers with a marked decrease in serum TP, albumin, and TG levels with decreased AchE and Paraoxonase activity. Additionally, malondialdehydes, nitric oxide (nitrite), 8-hydroxy-2-deoxyguanosine, and TNFα with a significant drop in the antioxidant activities were reported in the malathion group. Malathion upregulated the inflammatory cytokines and apoptotic genes, while Nrf2, Bcl2, and HO-1 were downregulated. Ginseng® and malathion co-treatment reduced malathion’s harmful effects by restoring metabolic indicators, enhancing antioxidant pursuit, lowering the inflammatory reaction, and alleviating pathological alterations. So, Ginseng® may have protective effects against hepatic and renal malathion-induced toxicity on biochemical, antioxidant, molecular, and cell levels

Evaluation of the Adsorption Efficacy of Bentonite on Aflatoxin M1 Levels in Contaminated Milk

The existence of aflatoxin M1 (AFM1) in raw milk results in economic losses and public health risks. This research aims to examine the capability of bentonite to adsorb and/or eliminate AFM1 from various raw milk types. In addition, the effects of numerous bentonites (HAFR 1, 2, 3 and 4) on the nutritional characteristics of the milk were studied. Our findings revealed that goat milk had the highest value of AFM1 (490.30 ng/L) in comparison to other milks. AFM1 adsorption was influenced by applying bentonite (0.5 and 1 g) in a concentration-dependent manner for different time intervals (from 0 to 12 h). The percentage of AFM1 reached the maximum adsorption level after 12 h to 100, 98.5 and 98% for bentonites HAFR 3, 1 and 2, respectively. HAFR 3 (1 g bentonite) presented higher adsorption efficiency than other bentonites used in the phosphate buffer saline (PBS) and milk. Residual levels of AFM1 reached their lowest values of 0 and 1.5 ng/L while using HAFR 3 in PBS and milk, respectively. With regard to the influence of bentonite on the nutritional characteristics of milk, there was an increase in fat, protein and solid non-fat ratio while using HAFR 3 and 4, yet decreased lactose in comparison with the control. Scanning Electron Microscopy and Fourier Transform-Infrared Spectroscopy both identified bentonites as superior AFM1 binders. The results demonstrated that bentonite, particularly HAFR 3, was the most effective adsorbent and could thus be a promising candidate for the decontamination of AFM1 in milk