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- Radioactive Iodine-induced hypothyroidism interferes with the maturation
of reproductive organs during puberty in immature female rats-
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Abstract: Abstract Animal and human studies suggest that thyroid hormone may have critical roles in the development of the ovary. For example, thyroid deficiency disrupts the ovarian microarchitecture and menstrual cycle in neonate and adult women, respectively. Therefore, it is conceivable that thyroid deficiency might disrupt sexual maturation during the peri-pubertal period. To investigate the impact of radioactive iodine-induced thyroid deficiency on reproductive organs throughout puberty, immature female rats were given water containing radioactive iodine (0.37 MBq/g body weight) twice, on postnatal days 22 and 29. Radioactive iodine-induced hypothyroidism was revealed by low free thyroxin levels. Thyroid deficiency delayed the onset of vaginal opening, reduced ovarian weight and the number of medium-sized follicles and led to elongated uteri. However, there was no effect on the estrous cycle or absolute uterus weight. We conclude that radioactive iodine-induced thyroid deficiency delays sexual maturation and alters normal ovarian growth in peri-pubertal rats.
PubDate: 2022-08-09
- Augmented impulsive behavior in febrile seizure-induced mice
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Abstract: Abstract Febrile seizure (FS) is one of the most prevalent etiological events in childhood affecting 2–5% of children from 3 months to 5 years old. Debates on whether neurodevelopmental consequences rise in later life following a febrile seizure or not are still ongoing however there is limited evidence of its effect, especially in a laboratory setting. Moreover, the comparative study using both male and female animal models is sparse. To examine the effect of FS on the behavioral features of mice, both sexes of ICR mice were induced with hyperthermic seizures through exposure to an infrared heat lamp. The mice were divided into two groups, one receiving a single febrile seizure at postnatal day 11 (P11) and one receiving three FS at P11, P13, and P15. Starting at P30 the FS-induced mice were subjected to a series of behavioral tests. Mice with seizures showed no locomotor and motor coordination deficits, repetitive, and depressive-like behavior. However, the FS-induced mice showed impulsive-like behavior in both elevated plus maze and cliff avoidance tests, which is more prominent in male mice. A greater number of mice displayed impaired CAT in both males and females in the three-time FS-induced group compared to the single induction group. These results demonstrate that after induction of FS, male mice have a higher susceptibility to consequences of febrile seizure than female mice and recurrent febrile seizure has a higher chance of subsequent disorders associated with decreased anxiety and increased impulsivity. We confirmed the dysregulated expression of impulsivity-related genes such as 5-HT1A and tryptophan hydroxylase 2 from the prefrontal cortices of FS-induced mice implying that the 5-HT system would be one of the mechanisms underlying the increased impulsivity after FS. Taken together, these findings are useful in unveiling future discoveries about the effect of childhood febrile seizure and the mechanism behind it.
PubDate: 2022-07-29
- The preventive effect of Mori Ramulus on oxidative stress-induced cellular
damage in skeletal L6 myoblasts through Nrf2-mediated activation of HO-1-
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Abstract: Abstract The aim of the present study is to investigate the preventive effect of water extract of Mori Ramulus (MRWE) on oxidative stress-mediated cellular damages in rat skeletal L6 myoblasts. Our results demonstrated that MRWE pretreatment markedly improved cell survival and suppressed cell cycle arrest at the G2/M phase and apoptosis in hydrogen peroxide (H2O2)-treated L6 cells. H2O2-triggered DNA damage was also notably reduced by MRWE, which since it was correlated with protection of reactive oxygen species (ROS) production. Additionally, H2O2 stimulated cytosolic release of cytochrome c and up-regulation of Bax/Bcl-2 ratio, whereas MRWE suppressed these changes following by H2O2. Moreover, MRWE inhibited the cleavage of poly(ADP-ribose) polymerase as well as the activity of caspase-3 by H2O2. Furthermore, MRWE enhanced H2O2-mediated expression of nuclear factor erythroid 2-associated factor 2 (Nrf2) and its representative downstream enzyme, heme oxygenase-1 (HO-1). However, the protective effects of MRWE on H2O2-induced ROS production, cell cycle arrest and apoptosis were significantly attenuated by HO-1 inhibitor. In conclusion, our present results suggests that MRWE could protect L6 myoblasts from H2O2-induced cellular injury by inhibiting ROS generation along with Nrf2-mediated activation of HO-1, indicating this finding may expand the scope of application of Mori Ramulus in medicine.
PubDate: 2022-07-22
- Algorithm for environmental risk assessment of cosmetics to reduce their
environmental impact-
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Abstract: Abstract Cosmetics, especially rinse-off personal care products (PCPs), such as shampoo, facial cleanser, and body wash, are composed of various chemicals and are one of the sources of chemicals released into aquatic ecosystems. Therefore, the cosmetic industry strives to reduce the impact of their products on the aquatic environment. In this study, we proposed an algorithm based on persistence, bioaccumulation potential, and toxicity (PBT) for the environmental risk assessment of cosmetics. PBT features are generally used in the evaluation of the environmental impact of chemicals. Based on the PBT assessment, it is possible to predict the short- and long-term effects of chemicals on the environment. Our algorithm derives substance and product scores from PBT features, allowing for the risk assessment of each ingredient in the product. Furthermore, we proposed a criterion for the environmental impact grade through which each component can be classified. We intend to use this grade and factors determined through the algorithm to manufacture products with low environmental impact.
PubDate: 2022-07-19
- Chemokine expression in human 3-dimensional cultured epidermis exposed to
PM2.5 collected by cyclonic separation-
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Abstract: Abstract Fine particulate matter (PM2.5) exposure has a risk of inducing several health problems, especially in the respiratory tract. The skin is the largest organ of the human body and is therefore the primary target of PM2.5. In this study, we examined the effects of PM2.5 on the skin using a human 3-dimensional cultured epidermis model. PM2.5 was collected by cyclonic separation in Yokohama, Japan. Global analysis of 34 proteins released from the epidermis revealed that the chemokines, chemokine C-X-C motif ligand 1 (CXCL1) and interleukin 8 (IL-8), were significantly increased in response to PM2.5 exposure. These chemokines stimulated neutrophil chemotaxis in a C-X-C motif chemokine receptor 2-dependent manner. The oxidative stress and signal transducer and activator of transcription 3 pathways may be involved in the increased expression of CXCL1 and IL-8 in the human epidermis model. Interestingly, in the HaCaT human keratinocyte cell line, PM2.5 did not affect chemokine expression but did induce IL-6 expression, suggesting a different effect of PM2.5 between the epidermis model and HaCaT cells. Overall, PM2.5 could induce the epidermis to release chemokines, followed by neutrophil activation, which might cause an unregulated inflammatory reaction in the skin.
PubDate: 2022-07-14
- Repeated oral dose toxicity and genotoxicity of a standardized Quisqualis
indica extract-
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Abstract: Abstract Quisqualis indica L. of Combretaceae family is a traditional medicine that is widely used for various gastrointestinal discomfort including stomach pain, constipation, and digestive problem. In this study, the potential repeated dose toxicity and genotoxicity of a standardized Quisqualis indica L. extract (HU033) were determined under good laboratory practice conditions. For the repeated dose toxicity test, HU033 was orally administered to Sprague–Dawley (SD) rats at doses of 500, 1000, and 2000 mg/kg/day for 13 consecutive weeks. The genotoxicity of HU033 was determined with a standard battery of genotoxicity test, including an in vitro bacterial reverse mutation test, an in vitro chromosomal aberration test, and an in vivo micronucleus test. After 13 weeks of repeated dose of HU033 by oral administration, there was no treatment related adverse clinical sign including food consumption, organ weights, and histopathological findings or significant decrement in bodyweight. The no-observed-adverse-effect level of HU033 was higher than 2000 mg/kg in both male and female SD rats. No target organs were identified. In addition, no evidence of HU033 genotoxicity was detected based on results from the bacterial reverse mutation test, chromosomal aberration test, and micronucleus test. Based on results of this study, HU033 could be safely used in food and medical products within the tested dose range.
PubDate: 2022-07-08
- Policosanol suppresses tumor progression in a gastric cancer xenograft
model-
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Abstract: Abstract Gastric cancer (GC) is the most common cancer worldwide and the third leading cause of cancer death, with the fifth highest incidence. The development of effective chemotherapeutic agents is needed to decrease GC mortality. Policosanol (PC) extracted from Cuban sugar cane wax is a healthy functional food ingredient that helps improve blood cholesterol levels and blood pressure. Its various physiological activities, such as antioxidant, anti-inflammatory, and anticancer activities, have been reported recently. Nevertheless, the therapeutic efficacy of PC in gastric xenograft models is unclear. We aimed to investigate the anticancer effect of PC on human GC SNU-16 cells and a xenograft mouse model. PC significantly inhibited GC cell viability and delayed tumor growth without toxicity in the SNU-16–derived xenograft model. Therefore, we investigated protein expression levels in tumor tissues; the expression levels of Ki-67, a proliferation marker, and cdc2 were decreased. In addition, we performed proteomic analysis and found thirteen differentially expressed proteins. Our results suggested that PC inhibited GC progression via cdc2 suppression and extracellular matrix protein regulation. Notably, our findings might contribute to the development of novel and effective therapeutic strategies for GC.
PubDate: 2022-07-05
- Adrenergic blocker terazosin potentially suppresses acetaminophen
induced-acute liver injury in animal models via CYP2E1 gene-
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Abstract: Abstract Drug induced liver injury (DILI) is a global issue and acetaminophen (APAP) is considered as the main cause of this. Due to increasing incidents of DILI, current study attempted to investigate an alternative but better role of terazosin (alpha-adrenergic blocker) in APAP-induced acute liver injury in an animal model using New Zealand rabbits. APAP (1 g/kg of body weight) was given to New Zealand rabbits either with or without terazosin (0.5 mg/kg) and serum was collected after 4 h. Serum alanine transaminase (ALT), alkaline phosphatase (ALP) and ferritin level were determined to analyze the liver functioning of treated rabbits. Furthermore, total cholesterol (TC), total lipids (TL), high-density lipoproteins (HDL), low-density lipoprotein (LDL) and triglycerides (TG) levels were estimated to find any change in lipid profile of the treated animals. Moreover, the urea and creatinine levels assayed the actual renal functionality. To identify any modification in gene expression, qPCR of cytochrome P2E1 (CYP2E1) was performed. Terazosin in combination with APAP enhanced liver functioning by reducing the levels of liver injury markers viz. ALP and ALT, while lipid profile was also lowered by down regulation of TC, TL, LDL and TG with enhanced HDL levels. It caused significant down regulation of expression level of CYP2E1. It is concluded that terazosin has better effects induced on the recovery of normal liver functioning, by improving the liver profile, lipid profile and renal functioning both at tissue and molecular levels.
PubDate: 2022-07-01
- Fimbristylis ovata and Artemisia vulgaris extracts inhibited AGE-mediated
RAGE expression, ROS generation, and inflammation in THP-1 cells-
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Abstract: Abstract Advanced glycation end products (AGEs) can induce inflammatory signaling pathways through the receptor for AGEs (RAGE). Targeting RAGE could be a therapeutic strategy for treating chronic inflammation mediated by the AGE-RAGE axis. This study aimed to investigate the effects of Fimbristylis ovata and Artemisia vulgaris extracts on AGE-RAGE signaling and AGE-mediated oxidative stress and inflammation in THP-1 cells. F. ovata and A. vulgaris were extracted by a Soxhlet extraction, and antioxidant capacity was evaluated using DPPH and ABTS assays. The human monocytic cell line THP-1 was treated with AGE (600 µg/ml) with and without F. ovata and A. vulgaris extracts (100 µg/ml). The mitochondria-targeting antioxidant MitoQ (2 μg/ml) was used as a positive control. Cell viability, ROS generation, RAGE, AGE-RAGE signaling pathway components, and inflammatory cytokine levels were analyzed. F. ovata and A. vulgaris extracts showed antioxidative effects in non-cell-based assays. Treatment of THP-1 cells with AGE significantly increased the protein levels of RAGE and significantly increased the mRNA expression of cytokines, including TNF-α, IL-1β, and IL-6. AGEs induced the generation of ROS and levels of signaling molecules downstream of RAGE, including phosphorylated and total Erk1/2, JNK, and p38 MAPK, although not significantly. F. ovata and A. vulgaris extracts significantly decreased the protein levels of RAGE and significantly decreased the mRNA levels of cytokines. In conclusion, this study revealed that F. ovata and A. vulgaris extracts exert anti-inflammatory effects through the AGE-RAGE axis. However, details on this anti-inflammatory effect through AGE-RAGE signaling should be further investigated.
PubDate: 2022-07-01
- Effect of 3-caffeoyl, 4-dihydrocaffeoylquinic acid from Salicornia
herbacea on endothelial nitric oxide synthase activation via calcium
signaling pathway-
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Abstract: Abstract 3-Caffeoyl-4-dicaffeoylquinic acid (CDCQ) is a natural chlorogenic acid isolated from Salicornia herbacea that protects against oxidative stress, inflammation, and cancer. Nitric oxide (NO) plays a physiologically beneficial role in the cardiovascular system, including vasodilation, protection of endothelial cell function, and anti-inflammation. However, the effect of CDCQ on NO production and eNOS phosphorylation in endothelial cells is unclear. We investigated the effect of CDCQ on eNOS phosphorylation and NO production in human endothelial cells, and the underlying signaling pathway. CDCQ significantly increased NO production and the phosphorylation of eNOS at Ser1177. Additionally, CDCQ induced phosphorylation of PKA, CaMKII, CaMKKβ, and AMPK. Interestingly, CDCQ increased the intracellular Ca2+ level, and L-type Ca2+ channel (LTCC) blockade significantly attenuated CDCQ-induced eNOS activity and NO production by inhibiting PKA, CaMKII, CaMKKβ, and AMPK phosphorylation. These results suggest that CDCQ increased eNOS phosphorylation and NO production by Ca2+-dependent phosphorylation of PKA, CaMKII, CaMKKβ, and AMPK. Our findings provide evidence that CDCQ plays a pivotal role in the activity of eNOS and NO production, which is involved in the protection of endothelial dysfunction.
PubDate: 2022-07-01
- Semi-automated approach for generation of biological networks on
drug-induced cholestasis, steatosis, hepatitis, and cirrhosis-
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Abstract: Abstract Drug-induced liver injury (DILI) is one of the leading reasons for discontinuation of a new drug development project. Diverse machine learning or deep learning models have been developed to predict DILI. However, these models have not provided an adequate understanding of the mechanisms leading to DILI. The development of safer drugs requires novel computational approaches that enable the prompt understanding of the mechanism of DILI. In this study, the mechanisms leading to the development of cholestasis, steatosis, hepatitis, and cirrhosis were explored using a semi-automated approach for data gathering and associations. Diverse data from ToxCast, Comparative Toxicogenomic Database (CTD), Reactome, and Open TG-GATEs on reference molecules leading to the development of the respective diseases were extracted. The data were used to create biological networks of the four diseases. As expected, the four networks had several common pathways, and a joint DILI network was assembled. Such biological networks could be used in drug discovery to identify possible molecules of concern as they provide a better understanding of the disease-specific key events. The events can be target-tested to provide indications for potential DILI effects.
PubDate: 2022-07-01
- Mitoquinol mesylate (MITOQ) attenuates diethyl nitrosamine-induced
hepatocellular carcinoma through modulation of mitochondrial antioxidant
defense systems-
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Abstract: Abstract Diethyl nitrosamine (DEN) induced cirrhosis-hepatocellular carcinoma (HCC) model associates cancer progression with oxidative stress and mitochondrial dysfunction. This study investigated the effects of mitoquinol mesylate (MitoQ), a mitochondrial-targeted antioxidant on DEN-induced oxidative damage in HCC Wistar rats. Fifty male Wistar rats were randomly divided into five groups. Healthy control, DEN, and MitoQ groups were orally administered exactly 10 mg/kg of distilled water, DEN, and MitoQ, respectively for 16 weeks. Animals in the MitoQ + DEN group were pre-treated with MitoQ for a week followed by co-administration of 10 mg/kg each of MitoQ and DEN. DEN + MitoQ group received DEN for 8 weeks, then co-administration of 10 mg/kg each of DEN and MitoQ till the end of 16th week. Survival index, tumour incidence, hematological profile, liver function indices, lipid profile, mitochondrial membrane composition, mitochondrial respiratory enzymes, and antioxidant defense status in both mitochondrial and post-mitochondrial fractions plus expression of antioxidant genes were assessed. In MitoQ + DEN and DEN + MitoQ groups, 80% survival occurred while tumour incidence decreased by 60% and 40% respectively, compared to the DEN-only treated group. Similarly, MitoQ-administered groups showed a significant (p < 0.05) decrease in the activities of liver function enzymes while hemoglobin concentration, red blood cell count, and packed cell volume were significantly elevated compared to the DEN-only treated group. Administration of MitoQ to the DEN-intoxicated groups successfully enhanced the activities of mitochondrial F1F0-ATPase and succinate dehydrogenase; and up-regulated the expression and activities of SOD2, CAT, and GPx1. Macroscopic and microscopic features indicated a reversal of DEN-induced hepatocellular degeneration in the MitoQ + DEN and DEN + MitoQ groups. These data revealed that MitoQ intervention attenuated DEN-induced oxidative stress through modulation of mitochondrial antioxidant defense systems and alleviated the burden of HCC as a chemotherapeutic agent.
PubDate: 2022-07-01
- Toxicological and safety evaluations of Weissella cibaria strain CMU in
animal toxicity and genotoxicity-
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Abstract: Abstract Weissella cibaria belongs to the Lactobacillaceae family and has been isolated from traditional fermented foods and saliva of children with good oral health. Previous investigations have shown that W. cibaria CMU (Chonnam Medical University) is expected to be safe based on results of in silico and in vitro analyses. However, there is a lack of studies assessing its safety in vivo. A toxicological safety evaluation of W. cibaria CMU was performed using an acute oral safety study in rats, a 14-day oral range finding study, a subsequent 13-week oral toxicity study in rats and a genetic toxicity battery (in vitro bacterial reverse mutation, in vitro chromosome aberration in Chinese Hamster Ovary cells and in vivo micronucleus study in mice). The results of the studies in rats showed that the acute lethal dose of W. cibaria CMU is > 5000 mg/kg body weight (bw)/day (1.8 × 109 CFU/kg bw/day) and the 14-day or 13-week no observed adverse effect level (NOAEL) is 5000 mg/kg bw/day (1.8 × 109 CFU/kg bw/day), the highest dose administered. W. cibaria CMU was non-mutagenic in the bacterial reverse mutation test and non-clastogenic or aneugenic in vitro and in vivo. In conclusion, the toxicological studies performed demonstrated W. cibaria CMU to be a safe strain to consume. This study is the first study examining the potential of a W. cibaria strain to cause genetic toxicity and subchronic toxicity in rats according to the Organization for Economic Cooperation and Development guidelines.
PubDate: 2022-07-01
- Ameliorative effects of Dictyota dichotoma on hepatotoxicity induced by
gibberellic acid in albino rats-
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Abstract: Abstract Gibberellic acid (GA3) is a natural plant growth regulator that is crucial for plant structural and functional development. We examined the alleviating capacity of brown algae (Dictyota dichotoma) on biochemical and molecular degenerative processes caused by sub-chronic exposure to gibberellic acid resulting in hepatic cell apoptosis. Adult male albino rats were divided into five equal groups: the first group received distilled water, the second group was treated with GA3, the third group was administered D. dichotoma extract suspended in 1% carboxymethylcellulose (CMC), the fourth group was administered both GA3 and D. dichotoma simultaneously, and the fifth group received 1% CMC orally, 5 days per week for a total of 50 days. The results indicated that GA3 induced a significant increase in liver function parameters based on serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin, which indicate hepatotoxicity. A marked increase in malondialdehyde (MDA) levels and a marked decrease in reduced glutathione (GSH), glutathione-S-transferase (GST), and superoxide dismutase (SOD) were observed as a result of induction of lipid peroxidation and oxidative stress. Histopathology revealed severely degenerated hepatocytes including cytoplasmic vacuolations and many apoptotic cells with weak Bcl2 expression. Similarly, there was a significant up-regulation of gene and protein expression levels for the pro-apoptotic markers, Caspase-3 and Bax, and an increase in pro-inflammatory marker levels, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) as well as C-reactive protein (CRP). The co-administration of D. dichotoma restored the disrupted biochemical, histopathological, molecular, and inflammatory changes resulting from GA3 toxicity. Our results confirm the antioxidant, anti-inflammatory, anti-apoptotic, and hepatoprotective potential of D. dichotoma.
PubDate: 2022-07-01
- Short- and long-term effect of colorectal cancer targeting peptides
conjugated to gold nanoparticles in rats’ liver and colon after single
exposure-
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Abstract: Abstract Peptides play important roles in the diagnosis, prognostic predictors, and treatment of various kinds of cancer. Peptides (p.C, p.L and p.14), derived from the phage display peptide libraries, specifically binds to colorectal cancer (CRC) cells in vitro. To allow tumor specificity and selectivity for in vivo diagnosis of CRC, biotinylated p.C, p.L and p.14 were conjugated to AuNPs (14 nm) via the biotin-streptavidin interaction. Male Wistar rats were intravenously injected with a single dose (100 µg/kg body weight) of AuNPs (citrate-AuNPs, PEG-AuNPs, p.C-PEG-, p.L-PEG- and p.14-PEG-AuNPs). Animals were monitored for behavioral changes, and sacrificed either 14 days or 84 days post-injection. Biochemical changes, oxidative stress, and histology of the liver and colon were assessed. No significant changes were noted in the rats injected with all the AuNPs, except p.L-PEG-AuNPs that caused significant toxicity (p < 0.05) 14 days post-exposure when compared to control group, as evidenced by increased relative liver weight, increased malondialdehyde levels and histological changes in the liver. These changes, however, returned to normalcy 84 days post-injection. It can be concluded, based on these findings, that p.L induced a transient toxicity in rats after a single intravenous injection, and can therefore be considered non-toxic long-term after a single exposure.
PubDate: 2022-07-01
- Neurotoxicity of anthracene and benz[a]anthracene involves oxidative
stress-induced neuronal damage, cholinergic dysfunction and disruption of
monoaminergic and purinergic enzymes-
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Abstract: Abstract In this study, the modulatory effects of anthracene (ANT) and benz[a]anthracene (BEN) on biochemical markers associated with neurodegeneration were assessed in mouse hippocampal neuronal cells (HT-22). Neuronal cells were cultured and exposed to ANT and BEN (25–125 µM) for 5 days, and the cell viability was determined via MTT assay. Morphological characteristics of the cells were assessed using a compound microscope. Biochemical parameters such as acetylcholinesterase (AChE), monoamine oxidase (MAO) and adenosine deaminase (ADA) activities as well as oxidative stress biomarkers (catalase [CAT], glutathione -S- transferase [GST] activities and Glutathione [GSH] levels) and nitric oxide [NO] levels were assessed after cells were treated with ANT and BEN for two days. The results showed that cell viability reduced with an increase in exposure time. After the fifth day of treatment, BEN and ANT (125 µM) reduced percentage viability to 41 and 38.1%, respectively. Light micrographs showed shrinkage of cells, neuronal injury and cell death in cells treated with higher concentrations of BEN and ANT (50 and 125 µM). Furthermore, AChE and MAO activities reduced significantly after treatment for 48 h with ANT and BEN. A significant decrease in CAT and GST activities and low GSH levels were observed after treatment with BEN and ANT. However, both polycyclic aromatic hydrocarbons caused a significant increase in ADA activity and NO levels. These results suggest that ANT and BEN may induce neurodegeneration in neuronal cells via oxidative stress-induced-neuronal injury, disruption of cholinergic, monoaminergic and purinergic transmission, and increased nitric oxide levels.
PubDate: 2022-07-01
- Ameliorative or corrective effects of Fig “Ficus carica” extract on
nickel-induced hepatotoxicity in Wistar rats-
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Abstract: Abstract Many heavy metals and metalloids (e.g., Pb, Cd, and Ni) can contaminate the environment and cause severe health problems. Through this study, investigated the possible corrective effects of Ficus carica extract (FCE) against nickel (Ni) induced stress response and damage on the liver of rats. Male Wistar rats were divided into four groups (8 rats per group) and co-treated with FCE (350 mg/kg) and exposed to Nickel chloride (10 mg/kg) for 4 weeks. The volatile compounds of FCE were characterized by solid phase micro-extraction (SPME) coupled with GC–MS, and the biochemical parameters of stress were determined. The SPME–GC/MS analysis of FCE indicated the presence of thirty (30) phyto-bioactive compounds including alcohols, aldehydes, organic acids, ketones, furans, terpenes, ester and others. The best capacity for scavenging DPPH free radicals and metal chelating were found with the IC50 values of 0.49 and 2.91 mg/mL, respectively. Ni induced damage to various macromolecules. Malondialdehyde, protein carbonyls, alanine aminotransferase and gamma glutamyl transferarse levels were significantly increased in Ni exposed group compared to control group and co-treatment with FCE reduced the levels of these parameters. In conclusion, current findings showed that Ni-induced oxidative damage and the administration of FCE can improve correct and restore the alteration in the rat liver.
PubDate: 2022-07-01
- Effect of daflon-500®, a flavonoid compound on chlorpyriphos-induced
oxidative changes in the hypophysis and testes in adult male rats-
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Abstract: Abstract Alteration of redox status is one of the molecular pathways commonly associated with pesticide toxicity. Antioxidants, including those obtained from plant phenolics, have been shown to mitigate pesticide-induced cellular injury. The present study was aimed at evaluating the effect of daflon-500®, a flavonoid compound on sub-chronic chlorpyriphos-evoked changes in antioxidant and biochemical parameters in the hypophysis and testes of adult male rats. Twenty-five male albino rats were randomly divided into 5 groups of 5 animals each. Group I (DW) received distilled water (2 ml/kg); group II (SO) was dosed with soya oil (2 ml/kg); Group III (DAF) received daflon-500® at 1000 mg/kg ̴ 1/5th of LD50 (≥ 5000 mg/kg); group IV (CP) was administered chlorpyriphos at 7.74 mg/kg ̴ 1/10th of LD50 (77.4 mg/kg) while group V (DAF + CP) was previously treated with daflon-500® (1000 mg/kg) and then exposed to CP (7.74 mg/kg), 30 min later. Daily oral regimen administration was done for 60 days after which the animals were sacrificed by cervical venesection after light chloroform anesthesia. The hypophysis and testicular tissues were harvested, and their homogenates were analyzed for malondialdehyde, catalase and superoxide dismutase, and acetylcholinesterase levels. A significant increase in the hypophysis and testicular MDA concentrations, coupled with a decrease in the SOD, CAT, and AChE activities were observed in the CP group. The levels of these oxidative and biochemical parameters were alleviated in the group pretreated with Daflon-500®. Results of this study demonstrated that pre-treatment with Daflon-500® mitigated CP-induced alterations in oxidative and biochemical parameters apparently due to the antioxidant effect of the flavonoid compound.
PubDate: 2022-07-01
- Protective role of selenium on structural change of human hemoglobin in
the presence of vinyl chloride-
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Abstract: Abstract Vinyl chloride is a colorless gas with a pleasant odor capable of entering the body through oral or inhalation routes. Extensive studies on this compound indicated that it is a carcinogen, and Vinyl chloride exposure can result in a specific type of cancer in vinyl chloride workers. Whereas hemoglobin plays a vital role in oxygen transfer throughout the body, in a molecular aspect, the effect of vinyl chloride on human hemoglobin has not been studied. Furthermore, selenium as an antioxidant is a vital factor for the health of humans and animals. Then this research investigated the effect of the antioxidant capability of selenium at the same concentrations in blood on the interaction between vinyl chloride and hemoglobin. UV–visible, Fourier-transform infrared, chemiluminescence, and fluorescence spectroscopies were employed. The results indicated the destruction of hemoglobin structure in different concentrations of vinyl chloride. At the same time, the antioxidant effect of selenium inhibited the destructive impact of vinyl chloride on hemoglobin structure.
PubDate: 2022-06-25
- Phosphodiesterase 11 A (PDE11A), a potential biomarker for
glioblastoma-
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Abstract: Abstract Phosphodiesterase 11A (PDE11A), a 3′,5′-cyclic nucleotide phosphodiesterase, is a key regulator of intracellular signaling that functions by degrading cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). However, the function of PDE11A in brain tumors is currently unclear. In this study, we found that PDE11A may be involved in glioblastoma development. The protein and mRNA levels of PDE11A were significantly higher in U87-MG, U251-MG and U343-MG glioblastoma cell lines. Gene expression analyses by deep-sequencing revealed that PDE11A mRNA levels were higher in U87-MG and U251-MG cells compared to other cells in the cerebral cortex. A comprehensive analysis of The Cancer Genome Atlas (TCGA) data revealed that PDE11A expression was also elevated in glioblastoma patients. Taken together, these data indicate that PDE11A expression was increased in glioblastoma cell lines and glioma patients, suggesting that PDE11A could be a putative diagnostic marker and therapeutic target for glioma.
PubDate: 2022-04-12
DOI: 10.1007/s43188-022-00129-1
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