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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-1β, 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.

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.

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.

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 1/10 th LD 50 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.

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 (NFĸβ) within the renal tubules, while caused marked decrease of proliferating cell nuclear antigen (PCNA) immunostaining and transforming growth factor beta 1 (TGFβ 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.

Hepatotoxicity restricts the therapeutic benefit of many anti-tumor agents in clinic. Ifosfamide is a widely used antineoplastic drug which could cause toxicity of normal cells due to its toxic metabolites mainly via induction of oxidative stress. Regarding established antioxidant and anti-inflammatory potential of beetroot extract, we aimed to investigate its possible protective effect against ifosfamide-induced hepatotoxicity in the rat model through hematological, histopathological, biochemical, and immunohistochemical evaluation of oxidative and inflammatory biomarkers. A total of twenty-four male albino rats were divided into four groups: Group 1: served as control (Cont); Group II: beetroot extract (BRE); Group III: ifosfamide only (IFOS); Group IV: ifosfamide + beetroot extract (IFOS + BRE). Results of the present study revealed that ifosfamide administration caused hematological toxicity and liver injury evidenced by elevated serum ALT, AST, and ALP and decreased TP, and marked elevation of liver MDA and NO levels with depletion of GSH and reduction of SOD and CAT activities along with several deleterious histopathological and immunohistochemical alterations in liver tissue compared to control rats. Our findings suggest that co-treatment with BRE has showed considerable protection but not full protection against ifosfamide-induced toxicity and all markers showed a regression trend towards control values. The mechanism of this protection seems to be partially based on antioxidant and anti-inflammatory properties. Therefore, it is recommended to use beetroot extract as dietary natural supplement in the clinic to approve its benefit in patients undertaking ifosfamide therapy to minimize its toxicity.

Cisplatin (CP) as a potent chemotherapeutic agent is restricted due to its hepatotoxicity, nephrotoxicity, and multiple organ toxicity. The current study investigates the possible mechanisms responsible for the hepatorenal protective effects of ginger extract (GE) against cisplatin-induced hepatorenal toxicity in rats. Thirty-two male albino rats (240–250 g) were divided into four equal groups ( n  = 8) as follows: control group (single i.p. saline dose 7.5 ml/kg at the 15th day of the study), CP-treated group (7.5 mg/kg single i.p. injection of CP at the 15th day of the study), GE-treated group (500 mg/kg/ p.o daily for 20 days), and GE + CP-treated group (GE 500 mg/kg/day, p.o daily for 15 days prior to CP injection and 5 days after CP injection). At day 21st of the experiment, blood samples were collected, and serum was isolated for biochemical assessments. Then, rats were euthanized, and hepatic and renal tissues were collected for tissue biochemical parameters, histopathology, and immunohistochemistry evaluations. Cisplatin-injected rats showed marked alterations in the serum liver and kidney functions, oxidant/antioxidant biomarkers, pro-inflammatory cytokines; tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) and anti-inflammatory cytokine; interleukin-10 (IL-10). CP also induced overexpression of oxidative (INOS) and apoptotic (caspase-3) immunohistochemical markers in hepatic and renal tissues. Conversely, the combining administration of ginger extract before, with, and after CP treatment ameliorated the aforementioned biochemical, pathological, and immunohistochemical adverse effects induced by CP. In conclusion, ginger extract has protective effects against CP adverse effects, possibly via its antioxidant, anti-inflammatory, and anti-apoptotic properties.

The aim of this study was to investigate the existence of immune cells in uterine flush of repeat breeding Egyptian buffalo-cow ( Bubalus bubalis ) during follicular and luteal stages of estrous cycle. Furthermore, histopathological examination of fallopian tubes and uteri was conducted. A total of 30 reproductive tracts of buffalo-cow were obtained from a local slaughterhouse directly aft er slaughter. Collected genital tracts were transported to the laboratory within 1.5 h. Samples of uterine fluids were collected, centrifuged, stained and used for quantification of immune cells during follicular and luteal stages. Tissue specimens from fallopian tube (infundibulum, ampulla and isthmus) and uteri were used for histopathological examinations. Results showed up-regulation of luminal polymorphonuclear neutrophils (PMNs) and monocytes in the uterine flush samples of follicular stage compared to luteal stage. Reversely, eosinophils and lymphocytes were higher in luteal stage samples compared to follicular one. Histopathological examinations revealed purulent endometritis and chronic lymphocytic endometritis with disrupting of uterine architecture and massive inflammatory cells infiltration. Oviduct lesion revealed, chronic inflammation and sever chronic interstitial inflammation with disruption in microarchitecture of different regions of oviducts with inflammatory cells infiltrations. In a conclusion, endometrial and oviductal lesions represent a crucial problem in repeat breeding buffaloes. In addition, luminal uterine PMNs and monocytes were elevated in follicular stage of oestrous cycle. These findings, might explain in a part, loss of conception of repeat breeding buffaloes particularly those which did not express clear clinical signs of inflammations.

The present study aimed to investigate the protective effect of argan oil (AO) against nephrotoxic effects following overdose and long-term administration of betamethasone (BM). The phytochemical compositions of AO were assessed using GC/MS. Forty eight male Wister albino rats were divided into six groups and treated for 3 successive weeks. The control group was orally administrated distilled water daily, the BM group received BM (1 mg/kg, IM, day after day), AO/0.5 and AO/1 groups received AO (0.5 mL/kg, 1 mL/kg, orally, daily, respectively), BM + AO/0.5 group and BM + AO/1 group. The results revealed that BM induced hematological changes, including reduction of red blood cells with leukocytosis, neutrophilia, monocytosis, lymphocytopenia, and thrombocytopenia. Moreover, BM caused a significant increase of serum urea and creatinine levels, and renal malondialdehyde and nitric oxide contents with significant decrease of reduced glutathione content. BM also caused vascular, degenerative, and inflammatory histopathological alterations in kidney, along with an increase in the Bax/Bcl-2 ratio, activation of caspase-3, and decrease of proliferating cell nuclear antigen expression. Conversely, the concomitant administration of AO (0.5, 1 mL/kg) with BM ameliorated the aforementioned hematological, biochemical, pathological, and histochemical BM adverse effects. In conclusion, AO has protective effects against BM-induced renal damage, possibly via its antioxidant, anti-apoptotic, and proliferative properties.

This paper was published without table and figures.