Light and scanning electron microscopic characterization of the Egyptian buffalo hair in relation to age with analysis by SEM-EDX.

The purpose of this study was to demonstrate a relationship between the microstructure and measurements of Egyptian buffalo hair and age. The buffalo studied ranged in age from young to premature to adult (3-8 months, 1.5-3, 4-6, and 8-10 years). The hair was collected from the animals' withers. Cuticle elements were examined using scanning electron microscopy (SEM), light microscopy, and energy-dispersive X-ray (EDX) analysis. Hair shaft diameter increased with age, according to SEM and light microscopy measurements. The values of shaft diameter obtained by SEM of the same animal were 64%-67% of the values obtained by light microscopy due to shrinkage of the hair during the drying process. Additional microscopy measurements revealed that the width of the cortex and medulla increased with age, while the width of the cuticle decreased slightly. The medulla index of four different age groups ranged from 0.56 to 0.61 µm. The average distance between successive scale values increased from 4.83 µm in the young group to 8.86 µm between the ages of 8 and 10 years. The scale pattern had a distinct personality at each stage of age. The hair medulla was in the center and consisted of a mesh-like structure with large pores divided into smaller pores by septa. The cortex was a bundle of fibers that wrapped around the medulla. Light microscopy revealed small oval granules and large streak-like granules in the cortex. EDX spectra revealed that carbon, oxygen, and nitrogen were shown to be more abundant in all age groups of buffalo. In buffalo hair, oxygen was the second most abundant element after carbon. The carbon mass in the examined samples decreased slightly with age (42.31%, 39.18%, 38.88%, and 38.49%), while oxygen increased with age. We concluded that hair measurements varied with age, scale microstructure, and elements, so we estimated buffalo animals' ages up to 10 years. HIGHLIGHTS: The goal was to show a link between the microstructure and measurements of Egyptian buffalo hair and age. Hair shaft diameter increased with age, according to scanning electron microscopy (SEM) and light microscopy measurements. The hair shaft diameter obtained by light microscopy was higher than that obtained by scanning electron microscopy of the same animal; we hypothesized that the difference in hair shaft diameter measured by light microscopy and scanning electron microscopy of the same animal was due to the shrinkage of the hair during the drying process. The width of the cortex and medulla increased with age, while the width of the cuticle decreased slightly. The average distance between successive scale values increased from 4.83 µm in the young group to 8.86 µm between 8 and 10 years old. At each stage of age, the scale pattern had a distinct personality. Carbon, oxygen, and nitrogen were found to be more abundant in the hair of buffalo of all ages and were detected using energy-dispersive X-ray (EDX) spectra. After carbon, oxygen was the second most abundant element in buffalo hair. The carbon mass in the samples studied decreased slightly with age, while the oxygen mass increased. Hair measurements varied according to age, scale microstructure, and elements.

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.

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-ß 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.

Hepatorenal protective effect of nano-curcumin against nano­copper oxide-mediated toxicity in rats: Behavioral performance, antioxidant, anti-inflammatory, apoptosis, and histopathology.

BACKGROUND: Metal oxide nanoparticles (NPs) induce oxidative stress that can cause cellular toxicity. A natural antioxidant that can be used to protect tissues from oxidative stress is curcumin. PURPOSE: In the present study, we evaluated the protective effect of curcumin nanoparticles (curcumin-NPs) against copper oxide nanoparticles (CuO-NPs)-mediated hepatorenal effects on behavioral performance, biochemical markers, antioxidants, inflammation, apoptosis, and histopathology in rats. STUDY DESIGN: Twenty Wistar adult male rats were randomly divided into four groups (n = 5); Group Ι served as a control, group ΙΙ was orally gavaged with curcumin-NPs (100 mg/Kg), group ΙΙI orally received CuO-NPs (100 mg/kg), and group ΙV received both CuO-NPs and curcumin-NPs orally for 14 days. METHODS: Behavioral performance, biochemical markers, antioxidants, inflammatory mediators, and apoptotic gene expression were evaluated in addition to histopathological and immunohistochemical examination. RESULTS: The results revealed that rats exposed to CuO-NPs suffered from behavioral alterations and hepatic and renal damages, which indicated by a marked elevation of serum biochemical parameters, including alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, urea, uric acid, and creatinine and a decline of total protein. Moreover, there was a significant downregulation in the expression of antioxidants genes, whereas inflammatory mediators expression were upregulated. The histopathological and immunohistochemical examination also corroborated these findings. In contrast, rats co-treated with curcumin-NPs exhibited better behavioral performance, biochemical profile, gene expression, histological architecture, and immunohistochemical staining results. CONCLUSION: These findings strongly indicated that curcumin-NPs exert significant protection against the behavioral and hepatorenal disorders induced by CuO-NPs toxicity by modulating oxidative stress regulators and gene expression.

Protective effect of methylene blue against copper oxide nanoparticle-induced neurobehavioral toxicity.

Increasing attention has been paid in the past decade to assessing the toxicological effects of nanoparticles and finding a protectant; thus, the current study aimed to investigate the protective effect of the mitochondria-targeting drug methylene blue (MB) against copper oxide nanoparticle (CuO-NP)-induced neurobehavioral toxicity in rats. For this purpose, twenty rats were allocated to four equal groups (n = 5). The negative control group received distilled water intraperitoneally (IP) and Tween 80 (10 %) orally. The CuO-NP group was given a dose of 100 mg/kg of CuO-NPs, administered orally, and the positive control group was treated with 1 mg/kg MB intraperitoneally (IP). The final group was concurrently exposed to CuO-NPs and MB for 14 consecutive days. At the end of the study, each group was neurobehaviorally blind tested relative to other experimental animals, then brain tissue markers were determined and a histopathological examination was conducted. The results showed that supplementation with CuO-NPs induced neurobehavioral alterations; increased Cu content in the brain; and enhanced lipid peroxidation (malondialdehyde [MDA]), protein peroxidation (protein carbonyl [PC]), and DNA oxidative damage (8-hydroxy-2-deoxyguanosine [8-OH-dG]) compared to other treatments. In addition, a decrease was noted in the mitochondrial dehydrogenases' (aldehyde dehydrogenase 2 [ALDH2], and glutamate dehydrogenase [GDH]) activity in Cu-exposed rats. The histopathological findings revealed shrunken, pyknotic, and hypereosinophic cortical neurons and increased immune positive brown staining of caspase-3 protein, indicating apoptosis. Co-treatment with methylene blue ameliorated the neurotoxic effects of CuO-NPs; therefore, MB evidently had a powerful modulatory effect against the neurotoxicity of nano-Cu oxide via its antioxidant and mitochondrial protection properties.

Thiamethoxam induced hepatotoxicity and pro-carcinogenicity in rabbits via motivation of oxidative stress, inflammation, and anti-apoptotic pathway.

Thiamethoxam (TMX) is a non-mutagenic neonicotinoid insecticide that is widely used to combat different types of insects. The hepatotoxicity and carcinogenicity of TMX have been approved previously in mice but not in rats. However, the TMX-induced hepatotoxic and pro-carcinogenic effects on rabbits remain unclear. The present study elucidated the roles of oxidative stress, pro-inflammatory cytokines, and apoptosis-related genes in the hepatotoxic and carcinogenic effects of TMX on rabbits. Sixteen male rabbits were equally divided into two groups; eight rabbits orally treated with TMX at a dose of 250 mg/kg b.w for 90 successive days. Hepatotoxic effects of TMX were evidenced by attenuation of liver enzyme activities, elevation of bilirubin levels, and alterations in the hepatic architecture, including hepatocyte death by necrosis and apoptosis, lymphocyte infiltration and fibrosis. TMX induced oxidative stress, as evidenced by the significant increases in malondialdehyde levels and antioxidant enzyme (glutathione transferase and catalase) activities along with a decrease in glutathione levels. TMX also up-regulated the mRNA levels of interleukin-6 (1.6-fold) and B cell lymphoma-2 (1.8-fold) and down-regulated the mRNA level of the tumor necrosis factor-α (0.8-fold), indicating its effects on cell survival and proliferation through the inhibition of apoptosis. Interestingly, the elevated level of carcinoembryonic antigen and the appearance of ground glass-like hepatocytes suggested that TMX exerted a pro-carcinogenic effect. In conclusion, TMX exerts potentially hepatotoxic and pro-carcinogenic effects on rabbits by modulating oxidative/antioxidative status and pro-inflammatory cytokine production, inhibiting apoptosis and activating cell survival pathways.