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Ulcerative colitis (UC) is a chronic colonic inflammation with a significant health hazard. Aspergillus awamori (A. awamori ) is a microorganism with various bioactive compounds with natural antioxidant and anti-inflammatory properties. The present work aimed to elucidate the protective and therapeutic effects of varying concentrations of A. awamori against acetic acid (AA)-induced ulcerative colitis (UC) in rats. Nine groups of albino male rats were established: a control negative group (G1), a control positive group (G2,AA), and preventive protocol groups (including G3A, G4A, and G5A) that received 100 mg, 50 mg, and 25 mg/kg b.w, respectively, of A. awamori orally and daily from the 1st day of the experiment and for 7 consecutive days. Then, they were subjected to one dose of AA intrarectally on day 8th. G3B, G4B, and G5B were termed as curative protocol groups that received one dose of AA on day 8th and then administered 100 mg, 50 mg, and 25 mg/kg b.w. of A. awamori, respectively, on day 9th and continued receiving these doses daily until day 16th. Rats in the AA group exhibited marked histopathological alterations of the distal colon, with an exaggeration of the DAI. In addition, a remarkable increase in oxidative stress was represented by the elevation of MDA and NO levels with a decline in SOD and GPx activities. In addition, upregulation of TNF-α, IL-6, and IL-1β mRNA expressions and downregulation of Muc2 and Nrf2 levels were detected. Unambiguously, a remarkable anti-inflammatory effect was noticed either in A. awamori prevented or treated groups expounded by reducing and regulating TNF-α, IL-6, and IL-1β with improved pathological lesion scoring. The Muc2 , Nrf2 , and bcl-2 gene levels were upregulated and restored also. In summary, the findings in this work reveal that A. awamori supplementation successfully alleviated the UC induced by AA, which had a better effect when administered before colitis induction.

Fipronil (FIP) is a phenylpyrazole insecticide that is commonly used in agricultural and veterinary fields for controlling a wide range of insects, but it is a strong environmentally toxic substance. Exposure to FIP has been reported to increase the hepatic fat accumulation through altered lipid metabolism, which ultimately can contribute to nonalcoholic fatty liver disease (NAFLD) development. The present study aimed to examine the function of cerium oxide nanoparticles (CeNPs) in protecting against hepatotoxicity and lipogenesis induced by FIP. Twenty-eight male albino rats were classified into four groups: FIP (5 mg/kg/day per os), CTR, CeNPs (35 mg/kg/day p.o.), and FIP + CeNPs (5 (FIP) + 35 (CeNPs) mg/kg/day p.o.) for 28 consecutive days. Serum lipid profiles, hepatic antioxidant parameters and pathology, and mRNA expression of adipocytokines were assessed. The results revealed that FIP increased cholesterol, height-density lipoprotein, triacylglyceride, low-density lipoprotein (LDL-c), and very-low-density lipoprotein (VLDL-c) concentrations. It also increased nitric oxide (NO) and malondialdehyde (MDA) hepatic levels and reduced glutathione peroxidase (GPx) and superoxide dismutase (SOD) enzyme activities. Additionally, FIP up-regulated the fatty acid-binding protein (FABP), acetyl Co-A carboxylase (ACC1), and peroxisome proliferator-activated receptor-alpha (PPAR-α). Immunohistochemically, a strong proliferation of cell nuclear antigen (PCNA), ionized calcium-binding adapter molecule 1 (Iba-1), cyclooxygenase-2 (COX-2) reactions in the endothelial cells of the hepatic sinusoids, and increased expression of caspase3 were observed following FIP intoxication. FIP also caused histological changes in hepatic tissue. The CeNPs counteracted the hepatotoxic effect of FIP exposure. So, this study recorded an ameliorative effect of CeNPs against FIP-induced hepatotoxicity.

Healing of injuries caused by exposure to heat has been discussed in many studies, although a few drugs have been shown to produce satisfactory results. In this study, 100 healthy mice randomly allocated into four categories (each = 25 mice) were analyzed. A deep second-degree burn on the back of each mouse was created. The burns were dressed daily with either AgNPs or silver sulfadiazine over 28 days of treatment. Safety evaluation of the AgNP treatment was performed by measuring the deposition rate of silver in the liver, brain, and kidney of treated mice. In the murine burn model, the speed of wound healing and the antibacterial effect of AgNPs were better than those in the silver sulfadiazine group. Burn wounds treated with SSD appeared to display a greater degree of inflammation as notable by the three clinical signs of the inflammatory process such as redness and swelling which appeared to be less after wounds treated with AgNPs. Also, AgNP treatment modified leukocytic infiltration and reduced collagen degeneration in treated mice and enhanced healing processes that were confirmed by morphological and histological investigations. Beside the potential significant effects of AgNPs on reduction of some microorganism counts that routinely isolated from burn wounds included aerobic organisms as Staphylococcus aureus and Escherichia coli when compared to both SSD and control groups. The deposition kinetics of AgNPs revealed lower distribution in the liver, brain, and kidney than that in silver sulfadiazine-treated mice with respect to both SSD and control groups.

Some of pathogenic bacteria and fungi have the ability to produce fetal toxins which may be the direct causes of cytotoxicity or cellular dysfunction in the colonization site. Biological and non-biological environmental factors, challenge and microbes influence the effect of toxins on these pathogens. Modern research mentions that many natural materials can reduce the production of toxins in pathogenic microbes. However, researches that explain the mechanical theories of their effects are meager. This review aimed to discuss the ameliorative potential role of plant-derived compounds and probiotics to reduce the toxin production of food-borne microbes either in poultry bodies or poultry feedstuff. Moreover, studies that highlight their own toxicological mechanisms have been discussed. Adding natural additives to feed has a clear positive effect on the enzymatic and microbiological appearance of the small intestine without any adverse effect on the liver. Studies in this respect were proposed to clarify the effects of these natural additives for feed. In conclusion, it could be suggested that the incorporation of probiotics, herbal extracts, and herbs in the poultry diets has some beneficial effects on productive performance, without a positive impact on economic efficiency. In addition, the use of these natural additives in feed has a useful impact on the microbiological appearance of the small intestine and do not have any adverse impacts on intestinal absorption or liver activity as evidenced by histological examination.

The ubiquitous use of diazinon (DZN, an organophosphorus insecticide) has increased the probability of occupational, public, and the ecosystem exposure; these exposures are linked to negative health outcomes. The flavonoids curcumin (CUR) and quercetin (QUE) exert significant anti-inflammatory and antioxidant activities against toxicants, including insecticides. However, it is unclear whether their combination enhances these activities. Therefore, 40 albino rat were divided randomly into the CTR, DZN, CUR + DZN, QUE + DZN, and CUR + QUE + DZN groups, which are treated daily via gavage for 28 days. DZN induced neurohepatic inflammation and oxidative damage, which was confirmed by significant ( P  < 0.05) induction of aspartate and alanine aminotransferases, alkaline phosphatase, lactate dehydrogenase, γ-glutamyl transferase, and tumor necrosis factor-α and inhibition of acetylcholinesterase activity. Furthermore, the liver and brain of DZN-exposed rats exhibited a notable elevation in MDA level paralleled with reduction in antioxidant molecules, i.e., glutathione, superoxide dismutase, glutathione peroxidase, and catalase. The pretreatment of DZN-intoxicated rats with CUR or QUE substantially mitigated neurohepatic dysfunction and inflammation and improved liver and brain antioxidant status with reducing oxidative stress levels. Furthermore, pretreatment with CUR + QUE synergistically restored the neurohepatic dysfunction and oxidative levels to approximately normal levels. The overall results suggested that CUR or QUE inhibits DZN-mediated neurohepatic toxicity via their favorable anti-inflammatory, antioxidant, and free radical-scavenging activities. Moreover, both QUE and CUR may be mutual adjuvant agents against oxidative stress neurohepatic damages.

The incidence of adverse reactions in food is very low, however, some food products contain toxins formed naturally due to their handling, processing and storage conditions. 5-(Hydroxymethyl)-2-furfural (HMF) can be formed by hydrogenation of sugar substances in some of manufactured foodstuffs and honey under elevated temperatures and reduced pH conditions following Maillard reactions. In previous studies, it was found that HMF was responsible for harmful (mutagenic, genotoxic, cytotoxic and enzyme inhibitory) effects on human health. HMF occurs in a wide variety of food products like dried fruit, juice, caramel products, coffee, bakery, malt and vinegar. The formation of HMF is not only an indicator of food storage conditions and quality, but HMF could also be used as an indicator of the potential occurrence of contamination during heat-processing of some food products such as coffee, milk, honey and processed fruits. This review focuses on HMF formation and summarizes the adverse effects of HMF on human health.

Background Cadmium is a highly toxicant heavy metal that poses serious risks to aquatic organisms, animals, and humans. Recent studies have investigated using biological chitosan nanoparticles (Bio-CHNPs) as a potential solution to alleviate the harmful effects of Cd exposure, particularly in aquaculture. Bio-CHNPs have gained attention for their applications in drug delivery and biomedical research, indicating their potential utility in addressing environmental toxicity. Objective This research aims to explore the effectiveness of Bio-CHNPs in mitigating cadmium chloride (CdCL 2 ) toxicity in African catfish ( Clarias gariepinus). Methods One hundred and twenty (n = 120) catfish were divided into 4 groups; G1 (control); G2, intoxicated with 10% LC 50 of CdCL 2 ; G3 received 3 g/kg of Bio-CNPs; G4, treated with 10% LC 50 of CdCL 2 and Bio-CNPs 3 g/kg feed. Results CdCl 2 exposure resulted in severe liver, intestine, and kidney damage, which was evidenced by alterations in biochemical parameters, hormonal imbalance, DNA damage, and micronucleus formation. Antioxidant defense mechanisms were compromised, as the activities of Superoxide Dismutase (SOD), Total Antioxidant Capacity (TAC), and Catalase (CAT) were reduced. mRNA expression levels of inflammatory cytokines such as IL-1β, IL-8, and LBP were also significantly elevated following CdCl 2 exposure. Conversely, Bio-CHNPs treatment showed antioxidant and anti-inflammatory effects, greatly lowering the biochemical, genotoxic, and histopathological effects induced by CdCl 2 . Conclusion The outcomes of this study are indicative of the potential of Bio-CHNPs as a promising aquaculture feed supplement, with a dual advantage of antagonizing the toxicity of environmental pollutants like Cd and imparting antioxidant and immunomodulatory effects. Bio-CHNP supplementation can be a viable strategy for remedying aquatic environmental heavy metal pollution, with the ultimate safeguarding of human health and ecosystem balance.

Silver nanoparticles (AgNPs) are commonly utilized in medicine. However, they have negative effects on the majority of organs, including the reproductive system. AgNPs were reported to be able to reach the testicular tissues due to their nano size, which allows them to pass through blood-testicular barriers. The goal of this study was to see if alpha-lipoic acid (LA) or Ginkgo biloba (GB) might protect adult rat testes after intraperitoneal injection of AgNPs. Forty male healthy adult Wister albino rats were randomly assigned to four groups: control, AgNPs-intoxicated group intraperitoneally injected AgNPs 50 mg/kg b.w, 3 times a week; LA + AgNPs group intoxicated with AgNPs and orally gavaged with 100 mg LA/kg b.w; and GB + AgNPs group injected with AgNPs and orally given GB extract 120 mg/kg b.w for 30 consecutive days. Biochemical changes (testosterone, ACP, and prostatic acid phosphatase), oxidative indices, mRNA expression of proapoptotic (BAX) and anti-apoptotic (BCL-2) biomarkers, histological, and immunohistochemical changes in testicular tissues were investigated. Significant decrease in serum testosterone level and elevation in ACP and PACP enzyme activity in AgNPs-treated rats. As well, there were lowering in tGSH, GSH GR, GPx, and elevation in MDA and GSSG values. AgNPs-exposed rats expressed downregulation of testicular thirodexin-1 (Txn-1), transforming growth factor-1β (TGF-1β), anti-apoptotic (BCL-2), and upregulaion of proapoptotic biomarkers (BAX) mRNA expressions. Strong positive action to BAX and lowering the action of Ki-67 antibody were observed. Because of their antioxidant, anti-inflammatory, and anti-apoptotic properties, cotreatment with LA or GB could be beneficial in reducing the harmful effects of AgNPs on the testicles.

Background and Aim: Aflatoxins (AFs) are potent toxic metabolites produced from Aspergillus species. Whose existence in poultry ration leads to drastic economic losses, notably in duck, as the most susceptible poultry species. This study aimed to determine tissue residues of AFs, alterations in selected clinical chemistry variables in serum, mainly during the exposure period, and lycopene and silymarin's possible roles as herbal treatments against aflatoxicosis in Pekin duckling. Materials and Methods: The study used one hundred and twenty one-day-old Pekin ducklings and classified them into four groups comprising 30 ducklings in each group. The control group (G1) ducklings were fed a mycotoxin-free ration, and G2 received a naturally contaminated ration with 30 ppb of AFs. G3 and G4 consumed contaminated rations with AFs with 30 ppb for 2 weeks and were treated with lycopene 100 mg/kg or silymarin 600 mg/kg/food, respectively, for 10 days. Serum activities of alanine transaminase and alkaline phosphatase (ALP), glutamyl transferase, ALP, total protein and albumin creatinine and uric acid concentrations, oxidant/antioxidant parameters (malondialdehyde [MDA], total antioxidant capacity (TAC), glutathione S-transferase (GST), and catalase [CAT]), and hepatic AFs residue were determined. Lycopene and silymarin were used for the treatment of aflatoxicosis for another 10 days. Results: Hepatic and kidney parameters were elevated in the AFs intoxicated group and reduced in the lycopene- and silymarin-treated groups. They had elevated MDA and AFs residues with decreased antioxidant parameters (TAC, GST, and CAT) in the AFs group. At the same time, treatment with lycopene or silymarin had reversed the action of AFs on MDA, elevated the hepatic residue, and improved antioxidant activity. Conclusion: Lycopene and silymarin, with their potent antioxidant activity, can be used to reverse the harmful effects of AFs on hepatic and kidney tissue.

Heavy metals including cadmium (Cd) are one of the major persistent and non-biodegradable wastewater pollutants. However, Cd reaches the aquatic ecosystem via industrial and agricultural waste discharges and causes serious deterioration in the welfare status of aquatic animals. The use of feed supplements with immune-stimulants to mitigate the toxic influences of heavy metals including Cd is a much more intriguing point. Thus, the current experiment used the bio-synthetized chitosan nanoparticles derived from Bacillus subtilis (Bs-CNPs) as a feed supplement and evaluated its ameliorative impacts on the growth and welfare status of Cd-intoxicated Nile tilapia ( Oreochromis niloticus ). Bifactorial design (3 Bs-CNPs levels × 3 Cd levels) was used in the current study where Nile tilapia fingerlings (58–63 g) were fed on 0.0, 2, and 4 g Bs-CNPs/kg feed alongside with exposing to 0.0, 0.392, and 0.784 mg Cd/L for 60 days to represent nine treatments as follows: T1: control group (no Cd exposure; no Bs-CNPs supplement); T2 and T3: fish were intoxicated with 0.784 and 0.392 mg Cd/L, respectively; T4 and T5: fish fed on 2 and 4 g Bs-CNPs/kg feed, respectively; T6 and T7: fish were fed on 2 g Bs-CNPs/kg feed along with exposure to 0.784 and 0.392 mg Cd/L, respectively; and T8 and T9: fish were fed on 4 g Bs-CNPs/kg feed along with exposure to 0.784 and 0.392 mg Cd/L, respectively. It is noted that the Cd-intoxicated fish exhibited significant retardation in growth performance and digestive enzyme activities with a decline in their survival rate compared to the control group (T1). The results also revealed that exposing fish to Cd toxicity alone with no feed supplement (T2 and T3) experienced abnormal clinical signs and behavioral changes. Compared with the control group (no Cd with no Bs-CNPs), highest values of cortisol, glucose, aspartate and alanine aminotransferase, and acetylcholine esterase activity were found in fish fed on the control diet along with exposure to 0.784 mg Cd/L. Higher Cd restudies in liver, intestine, gills, kidney, and muscles tissues were detected in fish exposed to 0.784 mg Cd/L alone and the sequence order of Cd levels in different fish organs is intestine > gills > liver > kidney > muscles. Remarkable pathological alterations in hepatic and intestinal tissues were also observed. On the other hand, feeding Nile tilapia on Bs-CNPs-enriched diets alone with no Cd exposure enhanced their growth performance, digestive enzyme activities, and hematological parameters with no Cd residues in fish organs. Interestingly, feeding the Cd-intoxicated fish on diets with Bs-CNPs (4 g/kg feed) returned their growth, digestive enzymes, hematological, and biochemical parameters to approximate those of the control group. Furthermore, these treatments showed histopathological alteration recovery in the intestine and liver tissues is similar to those in the control group (no Cd with no Bs-CNPs). Fish fed on Bs-CNPs levels with no Cd exposure showed no Cd residues in different fish organs. The Cd levels in different organs of fish exposed to 0.392 mg Cd/L along with feeding on Bs-CNPs (4 g/kg feed) were lower than those in Cd-exposed fish treatments. Consequently, the current study evoked that feeding Nile tilapia fingerlings on Bs-CNPs (4 g/kg feed) could enhance their growth performance and protect the fish from the Cd toxicity that may occur in the aquatic ecosystem.