The effects of saline water consumption on sperm parameters, testicular histopathology, hormonal and antioxidants concentrations in Barki Rams.

The study aimed to assess the effects of water salinity on the sperm parameters, levels of cortisol, LH, FSH, testosterone and antioxidants as well as the testes' histopathology in Barki rams. Fifteen healthy Barki rams (1-1.5 years) were divided into three equal depending on the type of drinking water for nine months. The rams in the tap water group (TW, water that contained 350 ppm of total dissolved salts (TDS). Males in the high saline water group (HSW) were permitted to consume high saline water with 8,934 ppm TDS, whereas those in the second group were permitted to have moderately saline water (MSW, 4,557 ppm TDS). High salt concentration in drinking water had adverse effect on sperm viability, morphology and sperm cell concertation. Nitric oxide and malondialdehyde concentrations in blood were significantly higher in the MSW and HSW groups than in TW. There was a significant decrease in glutathione concentration as well as superoxide dismutase activity in TDS and HSW. Cortisol was most highly concentrated in the HSW, next in the MSW, and least in TW. The testosterone, LH, and FSH concentrations in the HSW and MSW groups were significantly lower than in TW. As the salt concentration in drinking water increases, damage to testicular tissue. The MSW group demonstrating vacuolation of lining epithelial cells with pyknotic nuclei in the epididymis and necrosis and desquamation of spermatogenic cells in seminiferous tubules while HSW group displaying desquamated necrotic cells and giant cell formation in the epididymis, as well as damage to some of the seminiferous tubules and showed congestion, vacuolation of spermatogenic epithelium of seminiferous tubules, and desquamated necrotic spermatogenic epithelium. In conclusion, the salinity of the water has detrimental impacts on the sperm morphology, viability and concentration, hormones and antioxidant levels in Barki rams.

Reproductive Injury in Male Rats from Acrylamide Toxicity and Potential Protection by Earthworm Methanolic Extract.

This study examined the protective effect of earthworm extract (EE) on acrylamide (ACR)-induced reproductive dysfunction. Forty male rats were allocated into four groups (n = 10). The G I (control) group received distilled water (D.W.). The G II group received ACR (5 mg kg-1 B.W. in D.W.) 5 days per week, orally, for 3 weeks. The G III group was administered EE (300 mg kg-1 B.W in D.W.) 5 days per week, orally, for 3 weeks. The G IV group was pretreated with EE for 3 weeks and then co-treated with EE and ACR for an additional 3 weeks. ACR decreased the number of sperm, sperm viability, and total motility. However, it increased testosterone levels with no effect on the FSH or LH levels. Moreover, ACR increased the concentrations of malondialdehyde (MDA) and nitric oxide (NO). Meanwhile, it decreased the glutathione (GSH) concentration in testicular tissues. Notably, the expression levels of p53 and Ki-67 were increased in the degenerated spermatogenic cells and in the hyperplastic Leydig cells of the testis of the ACR-treated group, respectively. Acrylamide induced alterations in the testicular tissue architecture. Interestingly, EE restored the sperm parameters and recovered the testicular histological structures and the biochemical alterations induced by ACR. In conclusion, earthworm extract ameliorated ACR-induced reproductive toxicity via restoring the testicular antioxidant balance and suppressing p53 and Ki-67 expressions in testicular tissues.

Astaxanthin Mitigates Thiacloprid-Induced Liver Injury and Immunotoxicity in Male Rats.

Thiacloprid (TCP) is a widely used neonicotinoid insecticide with a probable toxic hazard to animals and human beings. This hazard has intensified the demand for natural compounds to alleviate the expected toxic insults. This study aimed at determining whether astaxanthin (ASX) could mitigate the hepatotoxic effect of TCP and diminish its suppressive effect on immune responses in rats. Animals received TCP by gavage at 62.1 mg/kg (1/10th LD50) with or without ASX at 40 mg/kg for 60 days. Intoxicated rats showed modulation of serum transaminases and protein profiles. The hemagglutination antibody titer to sheep red blood cells (SRBC) and the number of plaque-forming cells in the spleen were reduced. The cell-mediated immunity and phagocytosis were suppressed, while serum interleukins IL-1ß, IL-6, and IL-10 were elevated. Additionally, malondialdehyde, nitric oxide, and 8-hydroxy-2'-deoxyguanosine levels were increased in the liver, spleen, and thymus, with depletion of glutathione and suppression of superoxide dismutase and catalase activities. The expressions of inducible nitric oxide synthase and the high mobility group box protein 1 genes were upregulated with histomorphological alterations in the aforementioned organs. Cotreatment with ASX markedly ameliorated the toxic effects of TCP, and all markers showed a regression trend towards control values. Collectively, our data suggest that the protective effects of ASX on the liver and immune system of TCP-treated animals depend upon improving the antioxidant status and relieving the inflammatory response, and thus it may be used as a promising therapeutic agent to provide superior hepato- and immunoprotection.

Biogenic and characterizations of new silver nanoparticles stabilized with indole acetic acid derived from Azospirillum brasilense MMGH-SADAT1, their bioactivity, and histopathological assessment in rats.

An Egyptian rhizobacterium Azospirillum sp. isolated from Sadat city was able to produce indole acetic acid (IAA) up to (30.59 µg/ml). The isolate was identified biochemically and by 16S rRNA sequencing which showed 99.9% similarity to Azospirillum brasilense. The new isolate has been registered in Genbank with accession number MH179119.1. Extracted IAA was used as reducing or stabilizing agent of sliver nanoparticles (AgNPs). Successful fabrication of biogenic IAA-AgNPs was confirmed by Fourier Transform Infrared Spectrophotometer (FTIR) analysis of IAA which showed absorbance peak at 3434.78 cm-1 due to the N-H stretch of primary amines. Highly resolution Transmission Electron Microscopy (HR-TEM) showed AgNPs coating or capping with IAA in spherical shaped with size ranged from 6.01 to 44.02 nm. Energy dispersive X-ray (EDX) analysis revealed that Ag+ ions were attached to the surface of IAA-AgNPs particles. HR-TEM examination showed cell wall damage of Citrobacter freundii cells after exposure to IAA-AgNPs leading to cell death. In vivo results showed that C. freundii infection of rats induced significant increase in liver and kidney functions and deleterious histopathological alteration in rat's tissues. However, treatment by extracted IAA and IAA-AgNPs could normalize the biochemical and histopathological alterations occurred in infected rats. This is the first study to prove that IAA extracted from Azospirillum brasilense is a hopeful capping agent for NPs which has potential to protect against pathogenic infections, nontoxic and/or safe on rat's metabolisms.

Ameliorative effects of jojoba oil on fipronil-induced hepatorenal- and neuro-toxicity: the antioxidant status and apoptotic markers expression in rats.

Jojoba (Simmondsia chinensis) is an economically important plant due to its high oil content in the seeds. Fipronil is an extensively used phenylpyrazole insecticide. The present investigation aimed to assess the possible ameliorative effect of jojoba oil on fipronil induced toxicity in rats. Animals orally received the insecticide dissolved in corn oil by stomach tube at 1/10th LD50 for 28 days. Fipronil induced hepatorenal toxic effects evidenced by elevated serum ALT, AST, ALP, and LDH activities, and urea and creatinine levels, with histomorphological changes in the liver and kidney. Brain GABA was elevated with histopathological alterations in the brain tissue. Oxidative stress was demonstrated in liver, brain, and kidney as indicated by elevated MDA and NO levels with reduction in GSH level and activities of SOD and CAT. In addition, caspase-3 gene expression was enhanced, while Bcl2 gene expression was downregulated in the three organs. Increased DNA fragmentation was recorded in the liver and kidney. Cotreatment of jojoba oil with fipronil ameliorated the toxic effects of fipronil on various organs with improvement of the antioxidant status, the rate of apoptosis and the histopathological alterations. In conclusion, jojoba oil provided significant protection against fipronil induced hepatorenal- and neuro-toxicity, by its antioxidant and antiapoptic effects, making it a possible beneficial protective of natural origin.

Ameliorative effects of corn silk extract on acetaminophen-induced renal toxicity in rats.

The current study aimed to investigate the protective effect of corn silk methanolic extract (CSME) against acetaminophen (APAP)-induced nephrotoxicity. The present study was carried out on 40 male Wistar albino rats, which were randomly divided into four groups (n = 10): control group, orally administered with a single dose of 1.8 ml 0.9% normal saline at the last day of the experiment; CSME group, orally received CSME (400 mg/kg BW daily for 5 weeks); APAP group, orally administered with a single dose of APAP (2 g/kg BW); and CSME and APAP group, orally administered with CSME, followed by a single oral dose of APAP. The results of this study revealed that APAP caused a significant increase in serum urea, creatinine concentrations, and malondialdehyde (MDA) concentrations in renal tissues. In addition, APAP caused a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities in renal tissues compared with the control group. Furthermore, APAP caused marked renal damage as revealed by alterations in histopathological architectures of kidney tissues. APAP resulted in a marked expression of caspase 3 and nuclear factor κB (NFĸß) within the renal tubules, while caused marked decrease of proliferating cell nuclear antigen (PCNA) immunostaining and transforming growth factor beta 1 (TGFß 1) expression within the epithelial lining of the renal tubules. However, pre-treatment with CSME returned all biochemical parameters, histopathological changes, and immunohistochemical parameters toward normal levels as the control group. In conclusion, oral administration of CSME protected rats against APAP renal toxicity through its antioxidant, anti-apoptotic, and anti-inflammatory protective mechanisms.