Effect of Substituting Soybean Meal in Oreochromis niloticus Diets with Pumpkin (Cucurbita maxima) Seed Cake on Water Quality, Growth, Antioxidant Capacity, Immunity, and Carcass Composition.

A 10-week feeding experiment was performed to determine the impacts of partial substitution of soybean meal (SB) with pumpkin seed cake (PSC) in Oreochromis niloticus diets on water quality, growth rate, antioxidant capacity, immunity, and carcass composition. One hundred and fifty tilapia fish (average weight, 11.93 ± 0.17 g) were randomly allocated to five diets. The first diet (the basal diet) contained 420 g of SB per kg of feed. The remaining four diets, namely, D1, D2, D3, and D4, had SB partially replaced by PSC at 10%, 20%, 30%, and 40%, respectively. The results revealed that D4 and D1 significantly improved dissolved oxygen levels, while water temperature, pH, total ammonia, and nitrate levels were not significantly affected. Replacing SB with PSC significantly improved specific growth performance indicators and feed conversion compared to the control, with the D4 group showing the best values. Increasing PSC levels decreased serum glucose, aspartate aminotransferase, alanine aminotransferase, cholesterol, and triglyceride levels. In contrast, the D4 group had higher globulin, albumin, total protein, and lysozyme serum levels. Moreover, fish-fed PSC had significantly increased superoxide dismutase, glutathione peroxidase, and catalase activities and significantly decreased malondialdehyde levels. Increasing PSC substitution levels in fish diets increased the ash and crude lipid contents in the bodies of the fish, while crude protein and moisture decreased. In conclusion, replacing SB with PSC in fish diets significantly enhances growth performance, feed conversion, and fish health. Moreover, the findings suggest that PSC can be a promising alternative protein source for sustainable aquaculture practices.

Influence of titanium dioxide nanoparticles and/or cadmium chloride oral exposure on testicular morphology, oxidative stress, and apoptosis in rats: Ameliorative role of co-enzyme Q10.

Background and objectives: Little is known about the implications of titanium dioxide nanoparticles (TiO2NPs) and cadmium chloride (Cd) co-exposure on the male reproductive system in mammals. As a result, this study researched the effects of oral TiO2NPs and/or Cd exposure on male reproduction and testicular functions. Additionally, a mitigation trial with co-enzyme Q10 (CoQ10) has also been conducted. Methods: In a 60-day experiment, seven experimental groups, each containing 10 male Sprague Dawley rats, were orally given distilled water (control), corn oil (vehicle control), CoQ10 (10 mg/kg b.wt), TiO2NPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TiO2NPs + Cd, and TiO2NPs + Cd + CoQ10. Then, sperm quality, male sex hormones, oxidative stress indications, Ti and Cd testicular residues, testes and accessory gland architecture, and apoptotic and inflammatory markers in rat testes were assessed. Results: TiO2NPs and/or Cd exposure negatively impacted body weight, weight gain, testicular weights, semen quality, serum reproductive hormones, oxidative stress parameters, and Caspase-3 and tumor necrosis factor (TNF-α) immunoreactions. Histopathological changes were recorded in testicular, seminal vesicle, and prostatic tissues. Yet, co-administration of CoQ10 with TiO2NPs and Cd substantially mitigated these adverse consequences. The most notable aspect is that it effectively lowered testicular tissue Ti and Cd levels. It also improved oxidant status, hormonal profile, and sperm picture. CoQ10 minimized the testicular damage implied by histological examination. Furthermore, CoQ10 significantly diminished TiO2NPs and Cd-induced Caspase-3 and TNF-α immunoexpression in testicular tissue. Conclusion: As a result, CoQ10 could be utilized as a safe remedy to protect male reproductive physiology from TiO2NPs and Cd damage.

The immunosuppressive, growth-hindering, hepatotoxic, and oxidative stress and immune related-gene expressions-altering effects of gibberellic acid in Oreochromis niloticus: A mitigation trial using alpha-lipoic acid.

This study aimed to examine the effects of gibberellic acid (GBA) on growth, hemato-biochemical parameters related to liver functions, digestive enzymes, and immunological response in Oreochromis niloticus. Besides, the probable underlying mechanisms were explored by assessing antioxidant, apoptotic, and immune-related gene expression. Furthermore, the likelihood of restoration following alpha-lipoic acid (LIP) dietary supplementation was explored. The fish (average initial weight 30.75 ± 0.46) were equally classified into four groups: the control group, the LIP group (fed on a basal diet plus 600 mg/kg of LIP), the GBA group (exposed to 150 mg GBA/L), and the GBA + LIP group (exposed to 150 mg GBA/L and fed a diet containing LIP and GBA) for 60 days. The study findings showed that LIP supplementation significantly reduced GBA's harmful effects on survival rate, growth, feed intake, digestive enzymes, and antioxidant balance. Moreover, the GBA exposure significantly increased liver enzymes, stress markers, cholesterol, and triglyceride levels, all of which were effectively mitigated by the supplementation of LIP. Additionally, LIP addition to fish diets significantly minimized the histopathological alterations in the livers of GBA-treated fish, including fatty change, sharply clear cytoplasm with nuclear displacement to the cell periphery, single-cell necrosis, vascular congestion, and intralobular hemorrhages. The GBA-induced reduction in lysozyme activity, complement C3, and nitric oxide levels, together with the downregulation of antioxidant genes (cat and sod), was significantly restored by dietary LIP. Meanwhile, adding LIP to the GBA-exposed fish diets significantly corrected the aberrant expression of hsp70, caspase- 3, P53, pcna, tnf-a, and il-1ß in O. niloticus liver. Conclusively, dietary LIP supplementation could mitigate the harmful effects of GBA exposure on fish growth and performance, physiological conditions, innate immunity, antioxidant capability, inflammatory response, and cell apoptosis.

Interactive effects of cadmium and titanium dioxide nanoparticles on hepatic tissue in rats: Ameliorative role of coenzyme 10 via modulation of the NF-κB and TNFα pathway.

This study investigated the effect of oral dosing of titanium dioxide nanoparticles (TNPs) and cadmium (Cd2+) on rat liver and the potential protective role of coenzyme Q10 (CQ10) against TNPs and Cd2+-induced hepatic injury. Seventy male Sprague Dawley rats were divided into seven groups and orally given distilled water, corn oil, CQ10 (10 mg/kg b.wt), TNPs (50 mg/kg b.wt), Cd2+ (5 mg/kg b.wt), TNPs + Cd2+, or TNPs + Cd2++CQ10 by gastric gavage for 60 successive days. The results showed that individual or mutual exposure to TNPs and Cd2+ significantly increased the serum levels of various hepatic enzymes and lipids, depleted the hepatic content of antioxidant enzymes, and increased malondialdehyde. Moreover, the hepatic titanium and Cd2+ content were increased considerably in TNPs and/or Cd2+-exposed rats. Furthermore, marked histopathological perturbations with increased immunoexpression of tumor necrosis factor-alpha and nuclear factor kappa B were evident in TNPs and/or Cd2+-exposed rats. However, CQ10 significantly counteracted the damaging effect of combined exposure of TNPs and Cd2+ on the liver. The study concluded that TNPs and Cd2+ exposure harm hepatic function and its architecture, particularly at their mutual exposure, but CQ10 could be a candidate protective agent against TNPs and Cd2+ hepatotoxic impacts.

Alpha-lipoic acid suppresses gibberellic acid nephrotoxicity in Nile tilapia (Oreochromis niloticus) via modulating oxidative stress, inflammation, cytokine production, and apoptosis.

Globally, gibberellic acid (GA) is one of the extensively used plant growth regulators in agriculture. Yet, there is limited information about their toxicity to fish. Recently, alpha lipoic acid (ALA) has drawn much interest due to its antioxidant properties. This study was planned to determine whether ALA might protect Nile tilapia's kidneys from the toxic effects of GA and the probable underlying mechanisms. Thus, 240 Oreochromis niloticus fish (average initial weight 30.67 ± 0.57) were allocated into four groups received a basal diet or a basal diet supplemented with 600 mg/kg ALA or a basal diet but exposed to a GA (150 mg/L), or ALA-fortified diet and concurrently exposed to GA as previously described. After 60 days, hematological, oxidative stress, lipid peroxidation, stress indices, selected kidney toxic byproducts, histological investigations, and associated gene expression were assessed. Anemia, leukopenia, hypoproteinemia, and elevated kidney function indicators were noticed in the GA-treated group. Additionally, there were detectable cortisol, glucose, 8-OHdG, and MDA increases. However, there was a considerable drop in Cat, Sod, Gpx, GSH, and AChE levels. Structural damage to the kidneys was also identified. In the kidney of fish treated with GA, pro-inflammatory cytokines (tnfα, il-1ß), stress, and apoptotic genes (hsp70, pcna, caspase-3, and p53) genes were markedly up-regulated, while anti-oxidative (cat, sod) gene expression was downregulated. Conversely, adding ALA to the diet abolished the GA-induced changes in most of the markers mentioned above. Conclusively, ALA protects against GA-induced hematotoxicity, oxidative damage, and nephrotoxic effects in Nile tilapia fish.

Restorative effects of gallic acid against sub-chronic hepatic toxicity of co-exposure to zinc oxide nanoparticles and arsenic trioxide in male rats.

Background and objectives: This study aimed to assess the effect of zinc oxide nanoparticles (ZNPs) and/or arsenic trioxide (ATO) exposure on the liver of adult male Sprague Dawley rats. Moreover, the probable ameliorative impact of gallic acid (GA) against ZNPs and ATO-induced hepatotoxicity and the possible underlying mechanisms were evaluated. Methods: Sixty male Sprague Dawley rats were distributed into six groups. The 1st and 2nd groups were orally given distilled water (1 ml/kg) and 20 mg GA/kg b. wt, respectively. The 3rd and 4th groups were orally given 100 mg ZNPs/kg b. wt and 8 mg ATO/kg b. wt, respectively. The 5th group was co-administered ZNPs and ATO at the doses mentioned above. The last one was co-administered ZNPs, ATO, and GA at the earlier described doses. All tested compounds were orally given once a day for 60 successive days. Then, serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total, direct, indirect bilirubin, triglycerides, total cholesterol, HDL, VLDL, and LDL were estimated. The hepatic content of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) was evaluated. Moreover, Bcl-2 and Bax's reactive proteins were immunohistochemically detected, and Zn and As residual patterns in hepatic tissues were assessed. Results: ZNPs, ATO, and ZNPs+ATO-exposed rats showed significantly (P < 0.001) elevated serum AST (219%, 233%, and 333%), ALT (300%, 400%, and 475%), ALP (169%, 205%, and 294%), and total bilirubin (42%, 68%, and 109%) compared to the control ones. On the other hand, a significantly (P < 0.001) declined SOD (58%, 49%, and 43%) and GPx (70%, 63%, and 56%) but increased MDA (133%, 150%, and 224%) was recorded in the hepatic tissues of ZNPs, ATO, and ZNPs+ATO exposed rats, respectively, relative to the control rats. Moreover, the hepatic tissues of the ZNPs, ATO, and ZNPs+ATO exposed rats showed a significant (P < 0.001) decrease in Bcl-2 (28%, 33%, and 23%) but elevation in Bax (217%, 267%, and 236%) immunoreactivities compared to the control rats. These findings were consistent with the microscopic alterations in the hepatic architecture and accumulation of Zn and As. Furthermore, a notable hyperlipidemic condition was recorded following ZNPs and/or ATO exposure. On the contrary, GA notably reduced hepatic enzymes compared to ZNPs+ATO-exposed rats. Additionally, GA markedly improved ZNPs+ATO-afforded liver tissue damage and apoptotic events. Conclusion: Overall, GA oral dosing significantly mitigated the negative effects of ZNPs and ATO on the liver by improving the antioxidant defense system and controlling apoptotic changes.

Neurobehavioral Responses and Toxic Brain Reactions of Juvenile Rats Exposed to Iprodione and Chlorpyrifos, Alone and in a Mixture.

Herein, male juvenile rats (23th postnatal days (PND)) were exposed to chlorpyrifos (CPS) (7.5 mg/kg b.wt) and/or iprodione (IPD) (200 mg IPD /kg b.wt) until the onset of puberty (60th day PND). Our results demonstrated that IPD and/or CPS exposure considerably reduced locomotion and exploration. However, CPS single exposure induced anxiolytic effects. Yet, neither IPD nor IPD + CPS exposure significantly affected the anxiety index. Of note, IPD and/or CPS-exposed rats showed reduced swimming time. Moreover, IPD induced significant depression. Nonetheless, the CPS- and IPD + CPS-exposed rats showed reduced depression. The individual or concurrent IPD and CPS exposure significantly reduced TAC, NE, and AChE but increased MDA with the maximum alteration at the co-exposure. Moreover, many notable structural encephalopathic alterations were detected in IPD and/or CPS-exposed rat brain tissues. The IPD + CPS co-exposed rats revealed significantly more severe lesions with higher frequencies than the IPD or CPS-exposed ones. Conclusively, IPD exposure induced evident neurobehavioral alterations and toxic reactions in the brain tissues. IPD and CPS have different neurobehavioral effects, particularly regarding depression and anxiety. Hence, co-exposure to IPD and CPS resulted in fewer neurobehavioral aberrations relative to each exposure. Nevertheless, their simultaneous exposure resulted in more brain biochemistry and histological architecture disturbances.

Toll-like receptors and nuclear factor kappa B signaling pathway involvement in hepatorenal oxidative damage induced by some food preservatives in rats.

Chemical food preservatives are extensively found in various processed food products in the human environment. Hence, this study aimed to investigate the effect of long-term exposure to five food preservatives (potassium sorbate (PS), butylated hydroxyanisole (BHA), sodium benzoate (SB), calcium propionate (CP), and boric acid (BA)) on the liver and kidney in rats and the probable underlying mechanisms. For 90 days, sixty male albino rats were orally given either water (control), 0.09 mg/kg b.wt BHA, 4.5 mg/kg b.wt PS, 0.9 mg/kg b.wt SB, 0.16 mg/kg b.wt BA, or 0.18 mg/kg b.wt CP. Liver and kidney function tests were assessed. Hepatic and renal oxidative stress biomarkers were estimated. Histologic examination analysis of liver and kidney tissues was achieved. Toll-like receptors 2 and 4 (TLR-2 and TLR-4), tumor necrosis factor-alpha (TNF-α), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) mRNA expression levels were measured. The results revealed that long-term oral dosing of the five food preservatives resulted in significant increases in alkaline phosphatase, alanine transaminase, aspartate transaminase, urea, uric acid, and creatinine levels. There were significant reductions in hepatic and renal antioxidant enzymes, an increase in MDA concentrations, and pathological alterations in renal and hepatic tissues. The mRNA levels of TLR-4, TLR-2, NF-κB, and TNF-α were elevated in the food preservatives-exposed groups. Conclusively, the current findings revealed that long-term exposure to PS, BHA, SB, CP, and BA has a negative impact on liver and kidney function. Furthermore, these negative effects could be mediated via oxidative stress induction, inflammatory reactions, and cytokine production.

Palliative effect of Moringa olifera-mediated zinc oxide nanoparticles against acrylamide-induced neurotoxicity in rats.

Repeated acrylamide (ACR) exposure in experimental animals and humans causes variable degrees of neuronal damage. Because of its unique features, several green synthesized nanomaterials are explored for neuromodulatory activity. Hence, this study investigated the effect of green synthesized zinc oxide nanoparticles using Moriga olifera leaves extract (MO-ZnONP) against acrylamide (ACR)-induced neurobehavioral and neurotoxic impacts in rat. Forty male Sprague Dawley rats were distributed into four groups orally given distilled water, MO-ZnONP (10 mg/kg b.wt), ACR (20 mg/kg b.wt), or MO-ZnONP + ACR for 60 days. Gait quality and muscular, motor, and sensory function were assessed. Acetylcholinesterase (AChE), dopamine, catalase, malondialdehyde (MDA), and Zn brain contents were determined. Brain histopathology and immunohistochemical localization of the amyloid-ß protein and abnormal Tau were performed. The results revealed that MO-ZnONP significantly reduced ACR-induced sensory dysfunctions, hind limb abnormality, and motor deficits. Additionally, the ACR-induced increase in dopamine and AChE were significantly supressed by MO-ZnONP. Besides, MO-ZnONP significantly restored catalase and Zn content but reduced increased MDA brain content resulting from ACR. Furthermore, the ACR-induced neurodegenerative changes and increased amyloid-ß and phosphorylated Tau immunoexpression was significantly abolished by MO-ZnONP. Conclusively, MO-ZnONP could be used as a biologically effective compound for mitigating ACR's neurotoxic and neurobehavioral effects.

Ameliorative effects of quercetin against hepatic toxicity of oral sub-chronic co-exposure to aluminum oxide nanoparticles and lead-acetate in male rats.

The present study was designed to evaluate the probable ameliorative role of quercetin (QCN) against oxidative hepatotoxicity induced by aluminum oxide nanoparticles (Al2O3NPs) with a diameter < 30 nm and lead acetate (Pb) co-exposure in adult male Sprague-Dawley rats. Rats were weighed and allocated to seven groups (n = 10 each) and were treated orally via orogastric gavage for 60 successive days: rats of the 1st group were kept as control given distilled water (1 ml/kg), rats of the 2nd group received 2 ml/kg BW/day corn oil; rats of the 3rd group were administered 20 mg/kg BW QCN/day; rats of the 4th group received 100 mg/kg BW Al2O3NPs; rats of the 5th group received 50 mg/kg BW Pb; rats of the 6th group co-received Al2O3NPs and Pb at the same previous doses; and rats of the 7th group were co-administered Al2O3NPs, Pb, and QCN at the same previous doses. At the end of the experiment, serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total, direct, indirect bilirubin, triglycerides, total cholesterol, HDL, VLDL, and LDL were estimated. The hepatic oxidative stress biomarkers as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPx), were also evaluated. Finally, the histopathological and histomorphometric evaluations and the residues of Al and Pb in hepatic tissues were assessed. Al2O3NPs and/or Pb exposure significantly elevated lipid peroxidation levels and considerably altered the hepatic biochemical parameters; nevertheless, QCN significantly reduced hepatic enzymes compared to toxicant exposed groups. Additionally, QCN significantly improved Al2O3NPs-afforded liver tissue damage, as established in microscopic findings on the liver in the group treated with Al2O3NPs + Pb. Conclusively, QCN could be a candidate natural agent to safeguard the liver versus the co-harmful impacts of Al2O3NPs and Pb toxicity.

Quercetin Abates Aluminum Trioxide Nanoparticles and Lead Acetate Induced Altered Sperm Quality, Testicular Oxidative Damage, and Sexual Hormones Disruption in Male Rats.

This study examined the effects of exposure to lead acetate (PbAc) and/or aluminum trioxide nanoparticles (Al2O3NPs) on testicular function. Additionally, the probable reproprotective effects of quercetin (QTN) against Al2O3NPs and PbAc co-exposure in male Sprague Dawely rats were assessed. Al2O3NPs (100 mg/kg b.wt.), PbAc (50 mg/kg b.wt.), and QTN (20 mg/kg b.wt.) were orally administered for 60 days. Then, spermiogram, histopathological examinations of the testis and accessory glands, and immunohistochemical detection of androgen receptors (AR) and tumor necrotic factor alpha (TNF-α) were achieved. Moreover, serum levels of male sex hormones and testicular levels of antioxidant indices were estimated. The results showed that Al2O3NPs and/or PbAc caused significant sperm abnormalities, testicular oxidative stress, and histopathological changes. Furthermore, serum testosterone, LH, and FSH levels significantly decreased, while estradiol levels significantly increased. The Al2O3NPs and/or PbAc co-exposed group had more obvious disturbances. Furthermore, QTN co-administration significantly reversed the Al2O3NPs and PbAc-induced testicular histopathological alterations, reduced antioxidant defenses, and altered AR and TNF-α immune expression in testicular tissues. Conclusively, Al2O3NPs and/or PbAc evoked testicular dysfunction by inducing oxidative injury and inflammation. However, QTN oral dosing effectively mitigated the negative effects of Al2O3NPs and PbAc by suppressing oxidative stress and inflammation and improving the antioxidant defense system.

Effects of Co-Exposure of Nanoparticles and Metals on Different Organisms: A Review.

Wide nanotechnology applications and the commercialization of consumer products containing engineered nanomaterials (ENMs) have increased the release of nanoparticles (NPs) to the environment. Titanium dioxide, aluminum oxide, zinc oxide, and silica NPs are widely implicated NPs in industrial, medicinal, and food products. Different types of pollutants usually co-exist in the environment. Heavy metals (HMs) are widely distributed pollutants that could potentially co-occur with NPs in the environment. Similar to what occurs with NPs, HMs accumulation in the environment results from anthropogenic activities, in addition to some natural sources. These pollutants remain in the environment for long periods and have an impact on several organisms through different routes of exposure in soil, water, and air. The impact on complex systems results from the interactions between NPs and HMs and the organisms. This review describes the outcomes of simultaneous exposure to the most commonly found ENMs and HMs, particularly on soil and aquatic organisms.