Nicotine exacerbates liver damage in a mice model of Ehrlich ascites carcinoma through shifting SOD/NF-κB/caspase-3 pathways: ameliorating role of Chlorella vulgaris.

Nicotine, a pervasive global environmental pollutant, is released throughout every phase of the tobacco's life cycle. This study examined the probable ameliorative role of Chlorella vulgaris (ChV) extract against nicotine (NIC)-induced hepatic injury in Ehrlich ascites carcinoma (EAC) bearing female Swiss mice. Sixty female Swiss mice were assigned to four equal groups orally gavaged 2% saccharin 0.2 mL/mouse (control group), orally intubated 100 mg ChV /kg (ChV group), orally intubated 100 µg/mL NIC in 2% saccharin (NIC group), and orally intubated NIC + ChV as in group 3 and 2 (NIC+ChV group). The dosing was daily for 4 weeks. Mice from all experimental groups were then inoculated intraperitoneally with viable tumor cells 2.5 × 106 (0.2 mL/mouse) in the fourth week, and the treatments were extended for another 2 weeks. The results have shown that NIC exposure significantly altered the serum levels of liver function indices, lipid profile, LDH, and ALP in the NIC-exposed group. NIC administration significantly increased hepatic inflammation, lipid peroxidation, and DNA damage-related biomarkers but reduced antioxidant enzyme activities. NIC exposure downregulated SOD1, SOD2, CAT, GPX1, and GPX2 but upregulated NF-κB hepatic gene expression. Notably, the presence of the EAC cells outside the liver was common in all mice groups. Liver tissue of the NIC-exposed group showed multifocal expansion of hepatic sinusoids by neoplastic cells. However, with no evidence of considerable infiltration of EAC cells inside the sinusoids or in periportal areas in the NIC + ChV groups. NIC significantly altered caspase-3, Bax, and BcL2 hepatic immune expression. Interestingly, ChV administration significantly mitigates NIC-induced alterations in hepatic function indices, lipid profile, and the mRNA expression of antioxidant and NF-κB genes and regulates the caspase-3, Bax, and BcL2 immunostaining. Finally, the in vivo protective outcomes of ChV against NIC-induced hepatic injury combined with EAC in female Swiss mice could suggest their helpful role for cancer patients who are directly or indirectly exposed to NIC daily.

Effects of extended dietary supplementation with Santalum album essential oil on hemato-biochemical changes, innate immune response, antioxidant status, and expression of related gene in Nile tilapia (Oreochromis niloticus).

The effects of long-term dietary supplementation with sandalwood (Santalum album L.) essential oil (SEO) was investigated on hemato-biochemical biomarkers, immune status, antioxidant capacity, and resistance against Staphylococcus aureus in Nile tilapia (Oreochromis niloticus). Five groups (with four replicates) of O. niloticus (12.60 ± 0.20 g) were fed diets supplemented with SEO at doses of 0, 0.5, 1.0, 2.0, and 4.0 mL/kg diet for 60 days. Results indicated a substantial increase in blood protein levels and lower serum cholesterol, cortisol, glucose, urea, creatinine levels and, transaminase activities of fish fed a 2.0-mL SEO/kg diet. Serum lysozyme activity, nitric oxide, complement-3 levels, and phagocytic activity were significantly improved in O. niloticus after 60 days of feeding SEO-supplemented diets. Dietary SEO at level of 2.0-mL SEO/kg diet increased the activities of SOD, CAT, and GPx, and decreased MDA levels in liver homogenate. In addition, dietary 2.0-mL SEO/kg diet significantly upregulated antioxidant genes expression (CAT, SOD, GPx, GST, and GSR) with downregulation of apoptotic genes (HSP70, TLR2, caspase-3, and PCNA) in the liver. Furthermore, SEO-enriched diets significantly down-regulated pro-inflammatory (TNF-α, IL-1ß, and IL-8) and up-regulated anti-inflammatory cytokine genes (TFG-ß and IL-10) in the spleen. Moreover, SEO fortification increased the relative percentage of survival against S. aureus challenge and regulated immune-antioxidant genes in the spleen after the challenge. Overall, the results revealed that long-term using SEO might strengthen the physiological performance, hepatic oxidant/antioxidant balance, innate immune response, and resistance of O. niloticus against bacterial infections.

The ameliorative effect of bergamot oil nano-emulsion in stressed rabbit bucks: Influence on blood biochemical parameters, redox status, immunity indices, inflammation markers, semen quality, testicular changes and the expression of HSPs genes.

This work explored the activities of bergamot oil nano-emulsion (NBG) in modulating blood biochemical parameters, redox status, immunity indices, inflammation markers, semen quality, testicular changes and the expression of HSPs genes in stressed rabbit bucks. Twenty-four mature rabbit bucks (5 months) were randomly divided into three groups; control group (NBG0) received 1 ml of distilled water, while the other two groups received NBG orally at doses of 50 and 100 mg/kg (bw) twice a week. The present study's findings revealed that treated groups had lower values of total and direct bilirubin, triglyceride, lactate dehydrogenase, and creatinine compared with NBG0 group (p < 0.05). NBG100 group recorded the greatest of total protein, albumin, GPx, T3 and T4 values as well as the lowest values of uric acid, MDA, and indirect bilirubin. Both treated groups showed significantly reduced 8-OhDG, Amyloid A, TLR 4, while significantly increased nitric oxide, IgA, IgM, TAC, and SOD levels. Semen characteristics such as volume, sperm count, sperm motility, normal sperm, and vitality were significantly higher in the NBG100 group compared to the NBG50 and NBG0 groups, whereas sperm abnormalities and dead sperm were significantly reduced. HSP70, HSP72, and HSPA9 gene overexpression showed that testicular integrity was maintained after buck received oral doses of 50 or 100 mg/kg of NBG. Existing findings indicate that oral administration of NBG improves heat tolerance in rabbit bucks primarily as e result of its antioxidant and anti-inflammatory effects.

Protective prospects of eco-friendly synthesized selenium nanoparticles using Moringa oleifera or Moringa oleifera leaf extract against melamine induced nephrotoxicity in male rats.

Nanotechnology is used in a wide range of applications, including medical therapies that precisely target disease prevention and treatment. The current study aimed firstly, to synthesize selenium nanoparticles (SeNPs) in an eco-friendly manner using Moringa oleifera leaf extract (MOLE). Secondly, to compare the protective effects of green-synthesized MOLE-SeNPs conjugate and MOLE ethanolic extract as remedies for melamine (MEL) induced nephrotoxicity in male rats. One hundred and five male Sprague Dawley rats were divided into seven groups (n = 15), including 1st control, 2nd MOLE (800 mg/kg BW), 3rd SeNPs (0.5 mg/kg BW), 4th MOLE-SeNPs (200 µg/kg BW), 5th MEL (700 mg/kg BW), 6th MEL+MOLE, and 7th MEL+MOLE SeNPs. All groups were orally gavaged day after day for 28 days. SeNPs and the colloidal SeNPs were characterized by TEM, SEM, and DLS particle size. SeNPs showed an absorption peak at a wavelength of 530 nm, spherical shape, and an average size between 3.2 and 20 nm. Colloidal SeNPs absorption spectra were recorded between 400 and 700 nm with an average size of 3.3-17 nm. MEL-induced nephropathic alterations represented by a significant increase in serum creatinine, urea, blood urea nitrogen (BUN), renal TNFα, oxidative stress-related indices, and altered the relative mRNA expression of apoptosis-related genes Bax, Caspase-3, Bcl2, Fas, and FasL. MEL-induced array of nephrotoxic morphological changes, and up-regulated immune-expression of proliferating cell nuclear antigen (PCNA) and proliferation-associated nuclear antigen Ki-67. Administration of MOLE or MOLE-SeNPs significantly reversed MEL-induced renal function impairments, oxidative stress, histological alterations, modulation in the relative mRNA expression of apoptosis-related genes, and the immune-expression of renal PCNA and Ki-67. Conclusively, the green-synthesized MOLE-SeNPs and MOLE display nephron-protective properties against MEL-induced murine nephropathy. This study is the first to report these effects which were more pronounced in the MOLE group than the green biosynthesized MOLE-SeNPs conjugate group.

Neurobehavioral and immune-toxic impairments induced by organic methyl mercury dietary exposure in Nile tilapia Oreochromis niloticus.

Although substantial knowledge of mercury toxicity in fish has been assembled; until now, studies investigating the toxic impacts in Nile tilapia (Oreochromis niloticus) following dietary exposure to organic methyl mercury (MeHg) are less prolific. Accordingly, the current study aimed to evaluate the impacts of MeHg on neurobehavioral and immune integrity in Nile tilapia after dietary exposure. Two hundred and twenty-five juvenile Nile tilapia (19.99 ± 0.33 g) were allocated into five groups in triplicates (15 fish/replicate). G1, G2, G3, G4, and G5. O. niloticus were fed corresponding basal diets containing 0, 0.5, 1, 1.5, and 2 mg/kg diet MeHg chloride (MeHgCl) daily for 30 days, zero value represented the control G1 group. The results showed that MeHg induced significant alterations in O. niloticus behavior, the swimming behavior was significantly decreased, while scratching, biting, and fin tugging behaviors were significantly augmented. Moreover; chasing, mouth pushing, and butting behaviors were significantly increased in all the exposed groups. MeHg significantly decreased brain acetylcholine esterase (AChE) and serum immunoglobulin M (IgM) levels in all the exposed groups. Meanwhile, serum levels of lysozyme (LYZ), nitric oxide (NO), superoxide dismutase (SOD) malondialdehyde (MDA), protein carbonyl (PCO), and 8 hydroxy 2 deoxyguanosine (8OH2dG) were significantly elevated in all the exposed groups except for serum reduced glutathione (GSH) content was significantly decreased implying oxidative stress (OS), lipid peroxidation (LPO), protein, DNA damage and impaired immune response of the exposed tilapia. MeHg significantly altered transcriptional expression of immune-related genes including (TNF-α, IL-1ß, and IL-8, and IL-10) in all the exposed groups. From the obtained outcomes, the present research is the premier to investigate that dietary MeHg exposure in O. niloticus significantly induced neurobehavioral and immune defense impairments in a dose-related manner. This study exhibits that dietary MeHg may pose a potential threat to the O. niloticus populations.

p53 inhibits the proliferation of male germline stem cells from dairy goat cultured on poly-L-lysine.

Male germline stem cells (mGSCs) can transmit genetic materials to the next generation and dedifferentiate into pluripotent stem cells. However, in livestock, mGSC lines are difficult to establish, because of the factors that affect their isolation and culture. The extracellular matrix serves as a substrate for attachment and affects the fate of these stem cells. Poly-L-lysine (PL), an extracellular matrix of choice, inhibits and/or kills cancer cells, and promotes the attachment of stem cells in culture. However, how it affects the characteristics and potentials of these stem cells in culture needs to be elucidated. Here, we isolated, enriched and cultured dairy goat mGSCs on five types of extracellular matrices. To explore the best extracellular matrix to use for culturing them, the characteristics and proliferation ability of the cells were determined. Results showed that the cells shared several characteristics with previously reported mGSCs, including the poor effect of PL on their proliferative and colony-forming abilities. Further examination showed upregulation of p53 expression in these cells, which could be inhibiting their proliferation. When a p53 inhibitor was included in the culture medium, it was confirmed to be responsible for the inhibition of proliferation in mGSCs. Optimal concentration of the inhibitor in the culture of these cells was 5 µM. Furthermore, addition of the p53 inhibitor increased the expression of the markers of self-renewal and cell cycle in goat mGSCs. In summary, suppressing p53 is beneficial for the proliferation of dairy goat mGSCs, cultured on PL.

Therapeutic applications of adipose-derived mesenchymal stem cells on acute liver injury in canines.

In this study, canine adipose-derived mesenchymal stem cells (cADSCs) therapeutic potential was investigated in artificially induced acute liver injury model by CCl4 in canines. The primary cADSCs cells were cultured and then intravenously administered into the canine animal model. Six cross-breed dogs were divided into three groups including blank control group, CCl4 model group, CCl4 induced cADSCs transplantation group. The results showed that after intraperitoneal injection of CCl4 solution, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and Albumin (ALB) in peripheral blood of experimental canines confirmed the correct induction of acute liver injury. Moreover, the liver structure showed clear macroscopic damage. The cADSCs were homed in the liver of the administered animals. The AST, ALT and ALB in the peripheral blood rapidly decreased. H&E and PAS histological evaluation showed that both the structure of canine liver tissue and the ability to synthesize hepatic glycogen could be restored to the control level after cADSCs transplantation. Therefore, cADSCs can play a therapeutic role in the recovery of liver injury. Overall, this study demonstrates that the primary cADSCs transplantation into the acute liver injury model induced by intravenous injection can play a certain therapeutic role in the recovery of liver in canines. These results may provide a new treatment idea for acute liver disease in pets clinically.

Amelioration of titanium dioxide nanoparticle reprotoxicity by the antioxidants morin and rutin.

The present study aimed to examine the ameliorative effects of morin and rutin on the reproductive toxicity induced by titanium dioxide nanoparticles (TiO2NPs) in male rats. A total of seventy adult male Sprague-Dawley rats were randomly divided into seven groups, each comprising ten rats. Nanoreprotoxicity was induced by treating rats with TiO2NPs at a dosage of 300 mg/kg body weight for 30 days. Morin (30 mg/kg body weight) and rutin (100 mg/kg body weight) were co-administered with or without TiO2NPs to rats either individually or combined. Only distilled water was administered to the control group. The results showed that TiO2NPs enhanced oxidative stress, indicated by reduced levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in testicular tissues, and increased levels of the lipid peroxidation marker malondialdehyde (MDA). TiO2NPs significantly reduced the levels of sex hormones (testosterone, FSH, and LH), reduced sperm motility, viability, and sperm cell count, and increased sperm abnormalities, in addition to damaging the testicular histological architecture. TiO2NPs resulted in the downregulation of 17ß-HSD and the upregulation of proapoptotic gene (Bax) transcripts in the testicular tissues. Conversely, morin and/or rutin had a protective effect on testicular tissue. They effectively counteracted TiO2NP-induced oxidative damage and morphological injury in the testis by conserving the endogenous antioxidant mechanisms and scavenging free radicals. Thus, we suggest that morin and rutin could be used to alleviate the toxicity and oxidative damage associated with TiO2NP intake.