Total Thiol Groups Research Articles

Potential therapeutic impacts of vitamin D on hypothyroid-induced heart and kidney fibrosis and oxidative status in male rat.

There are several interactions between thyroid hormones (THs) and kidney and heart function. Consequently, THs deficit results in profound changes in renal and cardiac function regulation. Interestingly, emerging evidence suggests that vitamin D (Vit D) may benefit to fibrotic lesions in various tissues. Herein, this study was designed to investigate the potential impact of Vit D on renal and cardiac fibrosis in hypothyroid rats. Forty male Wistar rats were divided into four groups as follow: control, hypothyroid (0.05% PTU in drinking water), and hypothyroid + Vit D (PTU and doses of 100 or 500 IU/kg/day, by gavage) groups. After 6 weeks, biochemical parameters such as creatinine and urea in serum samples, and oxidative stress markers including malondialdehyde (MDA), total thiol groups, and superoxide dismutase (SOD) in renal and cardiac tissues homogenate were measured. Also, renal and cardiac fibrosis was evaluated histologically using Masson's trichrome staining. Hypothyroidism significantly increased creatinine and urea. Also, in hypothyroid group renal and cardiac fibrosis as well as MDA were increased, while anti-oxidative markers including total thiol group and SOD were decreased. Administration of Vit D significantly improved these alterations in oxidative stress markers and fibrosis in renal and cardiac tissues. In conclusion, this study highlighted that Vit D supplementation reduced renal and cardiac fibrosis and improved oxidative stress. These results support the emerging experimental findings linking Vit D being introduced as a potential therapeutic agent.

An Oxidative Stress Study on Curcumin and NanoCurcumin against Aluminum Phosphide-induced Kidney Injury in Rats: The Role of SIRT1/FOXO3 Signaling Pathway in Nephrotoxicity.

In this study, we have investigated the aluminium phosphide (ALP) toxicity on Renal Function and oxidative stress in kidney tissue of male rats and the possible protective role of Curcumin and nanoCurcumin against ALP-induced nephrotoxicity. Thirty-six adult male rats were divided into 6 groups (n=6). ALP (2 mg/kg oral administration) and control groups received Curcumin and nanoCurcumin (oral administration 100 mg/kg) or without it. After seven days of treatment, kidney parameters, oxidative stress biomarkers, and expression level of sirtuins1 (SIRT1)/Forkhead box protein O1 (FoxO1) pathway genes were evaluated in kidney tissue. In addition, histopathological changes in the kidney tissues were assayed. In the ALP group, compared to the control group, lipid peroxidation levels, urea, and creatinine were increased, and total antioxidant capacity and thiol groups decreased significantly p < 0.05. In Curcumin and nanoCurcumin groups compared to the ALP group, lipid peroxidation and creatinine decreased significantly p < 0.05. Also, Curcumin and nanoCurcumin improved the tissue damage caused by ALP. NanoCurcumin modulated the effect of ALP on the gene expression levels in SIRT1/FoxO1. The present study showed that ALP intoxication in kidney tissue can induce oxidative damage. Moreover, Curcumin and nanocurcumin, as potential antioxidants, can be effective therapeutics in ALP-induced nephrotoxicity.

Pulmonary Protective Effects of Vitamin D and N-Acetylcysteine on Paraquat-Induced Lung Toxicity in Rats: Modulation of Oxidant / Antioxidant Balance

Background: Paraquat (PQ) is one of the most common herbicides used in agriculture that can lead to very acute toxicity in mammals. It has been reported that PQ has destructive effects on the lungs. Objective: We aimed to investigate the effect of N-acetyl Cysteine (NAC) and Vitamin D (Vit D) on the oxidative toxicity of the lung in subacute paraquat exposure. 36 male albino Wistar rats at 8 weeks were randomly divided into 6 groups (n=6). A control group, a PQ-intoxicated group (5 mg/kg body weight), a Vit D-treated group (2 μg/kg), an NAC-treated group, a PQ (6.25 mg/kg) + Vit D group, and finally a PQ + NAC group, each was treated for 7 days. Methods: In this experimental study, Lipid Peroxidation (LPO), Total Oxidant Status (TOS), Total Antioxidant Capacity (TAC), Total Thiol Groups (TTG), and Hydroxyproline (Hyp) levels in lung tissue were evaluated. Results: PQ exposure resulted in a substantial elevation of LPO, TOS, and Hyp levels. Conversely, TAC and TTG content demonstrably declined. Administration of either PQ+Vit D or PQ+NAC significantly reduced LPO, TOS, and Hyp levels in the PQ-exposed rats compared to the PQ group alone. Conversely, TAC and TTG content significantly increased in these groups. These findings suggest that both vitamin D and NAC may function as free radical scavengers and potential antioxidant agents, potentially alleviating the detrimental effects of PQ poisoning on the lungs. Conclusion: The present study has demonstrated the administration of Vit D and NAC to significantly mitigate PQ-induced lung injury in rats. This protective effect can be likely attributed to their modulation of the oxidant/antioxidant balance, as evidenced by reductions in LPO, TOS, and Hyp levels, alongside increases in TAC and TTG content. These findings suggest that vitamin D and NAC may function as free radical scavengers and antioxidant enhancers, offering protection against PQ-induced oxidative stress and subsequent lung tissue damage.

Molecular, Biochemical and Histological Assessment in Paraquat Induced Neurotoxicity: Restoring Role of Nano-curcumin in an Experimental Study

Abstract Background: Paraquat (PQ) is known to cause damage to various organs, including the brain. Although curcumin have anti-inflammatory and anti-oxidant properties, it is not yet clear how they relate to PQ-induced neurotoxicity. This study’s objective was to compare the effects of curcumin and nanocurcumin on PQ-induced neurotoxicity in male rats. Methods: 36 rats were randomly divided into 6 groups. control subjects and animals poisoned with PQ that received treatment with or without curcumin and nano-curcumin for 7 days. The brain tissues were collected at the end of this period. Total antioxidant capacity (TAC), lipid peroxidation (LPO), and total thiol groups (TTG) were assessed by using spectrophotometry. Moreover, the histopathology of brain and antioxidant gene expression were assessed by biochemical and reverse transcriptase polymerase chain reaction (RT-PCR) analysis. Results: Curcumin and nanocurcumin therapy alleviated the PQ-triggered oxidative stress in brain tissue by raising the levels of anti-oxidant biomarkers like TAC and TTG, up-regulating the expression of Nrf2, HO-1, and NQO-1, reducing the levels of oxidative stress indices like LPO, and down- regulating the expression of Keap-1 in brain tissue. Conclusions: Treatment with curcumin and nano-curcumin improves brain function in PQ toxicity and nanocurcumin was more advantageous than ordinary curcumin.

The protective effect of biotin supplementation and swimming training on cognitive impairment and mental symptoms in a rat model of Alzheimer's disease: A behavioral, biochemical, and histological study

Vitamin B (Vit B) plays a regulatory role in cognitive memory and learning. We examined the biochemical and behavioral effects of biotin supplementation (BS) and swimming training (ST) on Alzheimer's disease (AD), the most common type of dementia, in male rats. Sixty rats were randomly assigned to six groups: control, sham (receiving phosphate-buffered saline), AD (receiving a single injection of Aβ into the lateral ventricle), ST (for 28 days and before Aβ injection), and BS (receiving BS through oral gavage for 28 days before Aβ injection). The treatments were continued until the end of the behavioral tests. Learning and memory functions were investigated through the Morris water maze (MWM) and depression and anxiety-like behaviors were tested by elevated plus-maze (EPM) and forced swimming tests. In addition, oxidative stress biomarkers, such as total thiol groups (TTG) and malondialdehyde (MDA) in serum were assessed and histological studies were performed using brain tissues. In the AD group, Aβ increased the distance traveled and escape latency in the MWM, but co-administration of BS and ST attenuated the results of the MWM, EPM, and FST tests. Furthermore, BS decreased the litigious biochemical effects of Aβ by enhancing the levels of TTG, in addition to reducing serum MDA levels. The use of BS as a potent antioxidant improved Aβ-induced memory impairment. It attenuated oxidative stress biomarkers in the brain (number of Aβ plaques) and serum of AD rats. We provide evidence for the use of BS in neurodegenerative disorders, such as AD, to elucidate the possible mechanisms.

Cacao consumption improves passive avoidance memory impairment in a rat model of Alzheimer's disease: the role of hippocampal synaptic plasticity and oxidative stress.

Introduction: Alzheimer's disease (AD) causes progressive loss of cognitive function and synaptic plasticity, which is the most common form of dementia. The present study was designed to scrutinize the effects of cacao on passive avoidance memory function and to identify the roles of hippocampal synaptic plasticity and oxidative stress in an AD rat model induced by unilateral intracerebroventricular (UICV) injection of amyloid-beta (Aβ). Methods: Oral administration of cacao (500 mg/kg/ day) was given for 2 consecutive months. A memory retention test was conducted 24 h after passive avoidance training was completed. Subsequently, the amplitude of population spike (PS) and slope of field excitatory postsynaptic potentials (fEPSPs) were assessed at hippocampal long-term potentiation (LTP) in perforant pathway-dentate gyrus (PP-DG) synapses. Moreover, total thiol group (TTG) and malondialdehyde (MDA) concentrations were evaluated in the plasma. Furthermore, compact Aβ plaques were detected in the hippocampal DG by performing Congo red staining. Results: As a result of AD induction, passive avoidance memory was impaired; also, reduced fEPSP slopes, PS amplitudes, and content of TTG, and increase in MDA levels in the rats were observed. In contrast, cacao treatment ameliorated passive avoidance memory impairment, improved hippocampal LTP impairment, modulated oxidative-antioxidative status, and delayed Aβ plaques production in AD rats. Disscussion: Conclusively, cacao alleviates Aβ-induced cognitive deficit, probably by the amelioration of hippocampal LTP impairment, modulation of oxidative-antioxidative status, and inhibition of Aβ plaque accumulation.

Discovering the Potential Value of Coenzyme Q10 as an Adjuvant Treatment in Patients With Depression.

Depressive disorder or mental cold is the most common mental disorder, and depression exists all over the world and in all countries and cultures. The results of several studies have shown that using compounds with antioxidant properties has been fruitful in patients with depression. Coenzyme Q10 (CoQ10) is a fat-soluble antioxidant and exerts its antioxidant effect by directly neutralizing free radicals or reducing tocopherol and preventing the inhibition of mitochondrial activity because of oxidative stress. This study aimed to investigate the effects of oral CoQ10 in patients with depression as an adjunctive treatment. Sixty-nine patients with moderate and severe depression were randomly divided into 2 CoQ10 groups (36) and placebo (33). The first group of patients received CoQ10 supplements at a dose of 200 mg daily for 8 weeks along with standard interventions and treatments for depression, and the second group received standard treatments for depression along with a placebo. The change in the score of Montgomery-Åsberg Depression Rating Scale depression scale was evaluated 4 and 8 weeks after the intervention. Also, at baseline and 8 weeks later at the end of the study, serum levels of total antioxidant capacity, total thiol groups, nitric oxide, malondialdehyde, and interleukin 6 were assessed. The changes in the depression score at the end of the study showed that, in the group receiving the CoQ10 supplement after 8 weeks, there was a reduction in depression symptoms, which was statistically significant compared with before the start of the study Meanwhile, no significant changes were observed in the patients of the placebo group in terms of symptom reduction. Compared with baseline and the placebo condition, serum levels of nitric oxide and total thiol groups significantly decreased and increased, respectively. Also, no statistically significant changes were observed for interleukin 6, malondialdehyde, and total antioxidant capacity. A dose of 200 mg of CoQ10 supplement daily for 8 weeks can reduce depression and fatigue, as well as improve the quality of life of patients with depression. In addition, CoQ10 can significantly improve inflammation and oxidative stress status in patients with depression.

The Protective Effects of High-Intensity Interval Training Combined with Q10 Supplementation on Learning and Memory Impairments in Male Rats with Amyloid-β-Induced Alzheimer's Disease.

Oxidative stress plays a major role in the progression of Alzheimer's disease (AD)-related cognitive deficits. This study was done to determine the protective effects of coenzyme Q10 (CoQ10) and high-intensity interval training (HIIT) alone and in combination for eight continuous weeks, on oxidative status, cognitive functions, and histological changes in the hippocampus in amyloid-β (Aβ)-induced AD rats. Ninety male Wistar rats were randomly assigned to the sham, control, Q10 (50 mg/kg of CoQ10; P.O.), HIIT (high intensity: 4 min running at 85-90% VO2max, low intensity: 3 min running at 50-60% VO2max), Q10 + HIIT, AD, AD+Q10, AD+HIIT, and AD+Q10 + HIIT groups. The results showed that Aβ injection reduced cognitive functions in the Morris water maze (MWM) test and recognition memory in the novel object recognition test (NORT), which was accompanied by a decrease in total thiol groups, catalase, and glutathione peroxidase activities, an increase in malondialdehyde levels, and neuronal loss in the hippocampus. Interestingly, pretreatment with CoQ10, HIIT, or both, could markedly improve the oxidative status and cognitive decline in the MWM and NOR tests, and hinder neuronal loss in the hippocampus of Aβ-induced AD rats. Therefore, a combination of CoQ10 and HIIT can improve Aβ-related cognitive deficits, probably through an amelioration in hippocampal oxidative status and prevention of neuronal loss.

Redox Homeostasis Alteration Is Restored through Melatonin Treatment in COVID-19 Patients: A Preliminary Study.

Type II pneumocytes are the target of the SARS-CoV-2 virus, which alters their redox homeostasis to increase reactive oxygen species (ROS). Melatonin (MT) has antioxidant proprieties and protects mitochondrial function. In this study, we evaluated whether treatment with MT compensated for the redox homeostasis alteration in serum from COVID-19 patients. We determined oxidative stress (OS) markers such as carbonyls, glutathione (GSH), total antioxidant capacity (TAC), thiols, nitrites (NO2-), lipid peroxidation (LPO), and thiol groups in serum. We also studied the enzymatic activities of glutathione peroxidase (GPx), glutathione-S-transferase (GST), reductase (GR), thioredoxin reductase (TrxR), extracellular superoxide dismutase (ecSOD) and peroxidases. There were significant increases in LPO and carbonyl quantities (p ≤ 0.03) and decreases in TAC and the quantities of NO2-, thiols, and GSH (p < 0.001) in COVID-19 patients. The activities of the antioxidant enzymes such as ecSOD, TrxR, GPx, GST, GR, and peroxidases were decreased (p ≤ 0.04) after the MT treatment. The treatment with MT favored the activity of the antioxidant enzymes that contributed to an increase in TAC and restored the lost redox homeostasis. MT also modulated glucose homeostasis, functioning as a glycolytic agent, and inhibited the Warburg effect. Thus, MT restores the redox homeostasis that is altered in COVID-19 patients and can be used as adjuvant therapy in SARS-CoV-2 infection.

Comparison of therapeutic effects of N-Acetylcysteine with pregabalin in improving the clinical symptoms of painful diabetic neuropathy: a randomized, double-blind clinical trial

ObjectivesPainful diabetic neuropathy (PDN) is highly prevalent and annoyingly in patients with diabetes. The aim of this study was to investigate the effects of oral N-acetylcysteine (NAC) compared to pregabalin in PDN.MethodsOne hundred two eligible patients with type 2 diabetes and PDN were randomly recievied pregabalin (150 mg/day) or N-Acetylcysteine (NAC) (600 mg/ twice a day) for 8 weeks. Mean pain score, Sleep interference score (SIS), Patient Global Impression of Change (PGIC), Clinical Global Impression of Change (CGIC), and also, serum levels of total antioxidant capacity (TAC), total thiol groups (TTG), catalase activity (CAT), nitric oxide (NO), and malondialdehyde (MDA) were assessed at baseline and at the end of the study.ResultsNAC was well tolerated in all patients. The decrease in mean pain scores and increase in SIS was similar between two groups. More improvement in PGIC and CGIC from the baseline was reported in NAC group. NAC, significantly, decreased serum levels of MDA, and NO, but increased TAC, TTG, and CAT. Pregabalin, significantly, decreased serum levels of MDA, and NO and increased TAC.DiscussionNAC is efficacious in alleviate symptoms of PDN which is probably related to its antioxidant effects.Trial registrationThe research protocol received approval from the Ethics Committee of Hamadan University of Medical Sciences (IR.UMSHA.REC.1397.137). The trial registry URL and number in Iranian Registry of Clinical Trials (IRCT): https://www.irct.ir/trial/33313, IRCT20180814040795N2 (Registration date: 2019-01-21, Retrospectively registered)

Urolithin a Partially Protects against Oxidative Damage Induced for Microcistyn-lr in C6 Cells.

Microcystin-LR (MIC-LR) is a toxin which the mechanism of intoxication involves oxidative stress. Urolithin A (URO-A) is a metabolic product from the colonic fermentation of ellagic acid with antioxidant potential. This study aimed to evaluate the putative protective effect of URO-A against MIC-LR toxicity in C6 cells. C6 cells were incubated with MIC-LR (1 and 10 μM) and/or URO-A (3, 30, 60 and 100 μM) for 24 h. MIC-LR induced reactive species (RS) generation, depletion of total thiol (SH) groups, and survival loss when compared with the control group. Also, at 10 μM, MIC-LR induced CAT activity inhibition. URO-A caused CAT activity inhibition and showed a trend to increase RS generation (60 and 100 μM) per se. URO-A at 3 μM completely attenuated the RS generation and the impairment in SH groups caused by MIC-LR. Our results demonstrated that URO-A might offer a protective effect against toxicity caused by MIC-LR in glial cells by restoring the levels of RS and thiol groups.

Protective Effects of Xanthine Derivatives Against Arsenic Trioxide-Induced Oxidative Stress in Mouse Hepatic and Renal Tissues.

In this study, the protective efficacy of pentoxifylline (PTX) as a xanthine derivative against arsenic trioxide (ATO)-induced kidney and liver damage in mice was investigated. Thirty-six mice were divided into six groups, receiving intraperitoneal injections of saline, ATO, PTX, or a combination for four weeks. Blood samples were analyzed for serum biochemistry, while hepatic tissue underwent examination for histopathological changes and assessment of oxidative stress markers and antioxidant gene expression through Real-Time PCR. ATO exposure significantly increased serum markers (creatinine, ALT, BUN, ALP, AST) and induced histopathological changes in the liver. Moreover, it elevated renal and hepatic nitric oxide (NO) and lipid peroxidation (LPO) levels, and reduced antioxidant enzyme expression (CAT, GSR, GPx, MPO, SOD), total thiol groups (TTGs), and total antioxidant capacity (TAC). Conversely, PTX treatment effectively lowered serum hepatic and renal markers, improved antioxidant markers, and induced histopathological alterations. Notably, PTX did not significantly affect renal and hepatic NO levels. These findings suggest that PTX offers therapeutic potential in mitigating liver and acute kidney injuries induced by various insults, including exposure to ATO.

Therapeutic potentials of N-acetylcysteine immobilized polyrhodanine nanoparticles toward acetaminophen-induced acute hepatotoxicity in rat.

N-acetylcysteine (NAC) is a recommended drug for treating acetaminophen (APAP) intoxication. Due to NAC's low bioavailability, this study aimed to use polyrhodanine (PR) nanoparticles (NPs) as a drug carrier to improve the effectiveness of NAC. After preparation and characterization of NAC loaded on PR, 30 rats were randomly divided into five groups of six. The first group (control) received normal saline. Groups 2-5 were treated with normal saline, PR, NAC, and NAC loaded on PR, respectively. The treatments were started 4 h after oral administration of APAP (2000 mg kg-1 ). After 48 h, the animals were anesthetized, and liver function indices and oxidative stress were measured in tissue and serum samples. The APAP administration can increase aminotransferases and alkaline phosphatase enzymes in serum, decreasing the total antioxidant capacity and thiol groups and increasing lipid peroxidation in liver tissue. Administration of PR-NAC could effectively improve the level of serum-hepatic enzymes, total antioxidant capacity and thiol groups, lipid peroxidation, and pathological changes in liver tissue in animals poisoned with APAP. PR-NAC has a significant therapeutic effect on preventing acute hepatotoxicity caused by APAP, and its effectiveness can be associated with an improvement in the oxidant/antioxidant balance of liver tissue.

The effect of olibanum on the rats with memory deficit induced by scopolamine.

Oxidative stress is an important contributor to Alzheimer's disease. Olibanum has therapeutic effects on various diseases. The effect of Olibanum on memory deficit induced by scopolamine (Sco) was challenged. Four groups were considered as (1) control (2) Sco, (3-4) Sco - Olib 100 and 200 mg/kg. Treatment by Olib or vehicle was done for two weeks. The third week was accompanied by the Morris water maze (MWM) and passive avoidance (PA) with Sco injection. On the last day, the brain and hippocampus were used for evaluation of the malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and a total thiol group. Sco increased the traveled time and distance to reach the hidden platform during five days of learning (p<0.01 - p<0.001) whereas it decreased the traveled time and distance (p<0.05- p<0.01) in the target area during the probe test of MWM. Sco also decreased delay time in the PA test (P<0.05 - P<0.001). Sco also decreased CAT, SOD, and thiol, whereas it, increased MDA in both the cortex and hippocampus (p<0.01 - p<0.001). Olib attenuated the impaired performance of the rats induced by Sco in MWM and PA tests. Olib reversed the increasing effects of Sco on MDA in both cortex and hippocampus and also reversed the attenuating effects of Sco on CAT, SOD, and thiol. Olib had an inhibitory effect on memory deficit induced by Sco probably through its anti-oxidant property.

Carvacrol improved learning and memory and attenuated the brain tissue oxidative damage in aged male rats

Introduction: Aging is an unavoidable process in the body that is accompanied by impaired tissue homeostasis and various changes. Carvacrol has attracted considerable attention for its wide range of pharmacological activities. Therefore, this study attempted to explore the protective effect of carvacrol in aged rats.Materiel and methods: The aged rats were given carvacrol (15 or 30 mg/kg/day) for 4 weeks. Morris water maze and passive avoidance tests were used to determine the learning and memory abilities of the rats. The hippocampus and cortex samples were taken for biochemical analysis.Results: In comparison to young control rats, aged control rats showed learning and memory deficits. There was improvement in the Morris water navigation test and passive avoidance test performance in the treatment groups versus the aged control group. An increment in malondialdehyde (MDA) and a decrease in total thiol groups in the hippocampus and cortex samples of aged control rats in comparison to the young control group were observed. Carvacrol decreased MDA levels and increased total thiol groups in the hippocampus and cortex samples of aged rats.Conclusion: Carvacrol improved learning and memory in aged rats, probably through its anti-oxidation effects.

Silymarin pretreatment protects against ethanol-induced memory impairment: Biochemical and histopathological evidence

BackgroundEthanol (Eth.) abuse induces memory impairment. Oxidative damage and apoptosis are considered the likely causes of memory impairment. Silymarin (Sil.) is a flavonoid isolated from the plant Silymarin marianum (milk thistle). While studies have reported the neuroprotective effect of Sil. against neurodegenerative processes, the precise mechanism of action of Sil. in Eth.-induced memory impairment remains unclear. MethodsTwenty-eight rats were equally divided into four groups: Control (saline 1 ml/rat); Sil. (200 mg/kg for 30 days); Eth. (2 g/kg/day for 30 days); and Sil. + Eth. Behavioral tests including inhibitory avoidance and open field were used to investigate memory and locomotion. Brain antioxidant parameters, including catalase, superoxide dismutase, total antioxidant capacity and total thiol group, plus oxidative parameters, including malondialdehyde and total oxidant status, followed by hippocampal apoptosis (Bax/Bcl2, cleaved caspase) and histopathological changes were evaluated in the groups. ResultsWhile the administration of Eth. impaired memory, Sil. significantly reversed Eth-induced memory deficits. Eth. administration also augmented brain oxidative and hippocampal apoptosis parameters. In contrast, a marked reduction in brain antioxidant and anti-apoptotic parameters was observed in the Eth. group. At the tissue level, hippocampal sections from Eth.-treated animals revealed severe neuronal damage. The administration of Sil. to Eth.-treated rats remarkably alleviated all the said Eth.-induced biochemical and histopathological effects. On the contrary, Sil. alone did not change the behavior and biochemical/molecular parameters. ConclusionThe memory-enhancing effect of Sil. in Eth.-induced demented rats may be partly mediated by the augmented antioxidant effects and amelioration of apoptotic and histopathological changes.

Effect of sub-dermal exposure of silver nanoparticles on hepatic, renal and cardiac functions accompanying oxidative damage in male Wistar rats

Silver nanoparticles (AgNPs) have been generally used due to their strong antibacterial, antiviral and antifungal and antimicrobial properties. However, their toxicity is a subject of sustained debate, thus requiring further studies. Hence, this study examines the adverse effects of the sub-dermal administered dose of AgNPs (200 nm) on the liver, kidney and heart of male Wistar rats. Thirty male rats were randomly distributed into six groups of five animals per group. Group A and D served as the control and received distilled water for 14 and 28 days respectively. Groups B and C were sub-dermally exposed to AgNPs at 10 and 50 mg/kg daily for 14 days while E and F were sub-dermally exposed to AgNPs at 10 and 50 mg/kg daily for 28 days. The liver, kidney and heart of the animals were collected, processed and used for biochemical and histological analysis. Our results revealed that the subdermal administration of AgNPs induced significant increased (p < 0.05) activities of aspartate aminotransferase (AST), alanine transferase (ALT), alkaline phosphatase (ALP), urea, creatinine, and malondialdehyde (MDA) while decreasing the levels of glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and total thiol groups in the rat tissues. Our findings suggest that the subdermal administration of AgNPs induced oxidative stress and impaired the hepatic, renal and cardiac functions of male Wistar rats.

Protective effect of flaxseed oil the on diazinon-induced hepatotoxicity in male rats

Here in, we investigated the possible hepatoprotective effects of flaxseed oil on Diazinon (DZN) induced oxidative stress in rat liver. Twenty-five adult male Wistar rats (180–200 g) were divided randomly into five groups: Control group (1 ml normal saline orally), DZN group (70 mg/kg/day, p.o.), flaxseed oil group (200 mg/kg/day, p.o.), and co- treatment groups (DZN 70 mg/kg/day plus flaxseed oil at doses of 100 and 200 mg/kg/day, respectively). Oxidative stress markers including liver and serum level of malondialdehyde (MDA), catalase (CAT), total antioxidant capacity (TAC), and total thiol group (TTG) were analyzed. Also liver function tests such as serum Alanine aminotransferases (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST) were evaluated. Hematoxylin and eosin (H&E) staining was used for liver histological study. Compared to control group, DZN significantly increased liver and serum level of MDA, CAT, TAC and TTG. Also, DZN increased serum ALT, AST, and ALP levels. Flaxseed oil consumption significantly improved oxidative stress status and liver functions tests. Theses effectiveness was completely dose dependent. Also, flaxceed oil ameliorates liver histopathological alterations induced by DZN. Our data demonstrated DZN induced liver toxicity through oxidative stress mechanisms. Flaxceed supplementation had liver protective effects by decreasing oxidative stress markers and improvement of antioxidative status. Also, flaxceed reduced the development of DZN-induced alterations in liver. It seems that flaxceed supplementation may have protective role in DZN-induced oxidative damage in hepatic tissues.

Prediction of detailed blood metabolic profile using milk infrared spectra and machine learning methods in dairy cattle

The adoption of preventive management decisions is crucial to dealing with metabolic impairments in dairy cattle. Various serum metabolites are known to be useful indicators of the health status of cows. In this study, we used milk Fourier-transform mid-infrared (FTIR) spectra and various machine learning (ML) algorithms to develop prediction equations for a panel of 29 blood metabolites, including those related to energy metabolism, liver function/hepatic damage, oxidative stress, inflammation/innate immunity, and minerals. For most traits, the data set comprised observations from 1,204 Holstein-Friesian dairy cows belonging to 5 herds. An exception was represented by β-hydroxybutyrate prediction, which contained observations from 2,701 multibreed cows pertaining to 33 herds. The best predictive model was developed using an automatic ML algorithm that tested various methods, including elastic net, distributed random forest, gradient boosting machine, artificial neural network, and stacking ensemble. These ML predictions were compared with partial least squares regression, the most commonly used method for FTIR prediction of blood traits. Performance of each model was evaluated using 2 cross-validation (CV) scenarios: 5-fold random (CVr) and herd-out (CVh). We also tested the best model's ability to classify values precisely in the 2 extreme tails, namely, the 25th (Q25) and 75th (Q75) percentiles (true-positive prediction scenario). Compared with partial least squares regression, ML algorithms achieved more accurate performance. Specifically, elastic net increased the R2 value from 5% to 75% for CVr and 2% to 139% for CVh, whereas the stacking ensemble increased the R2 value from 4% to 70% for CVr and 4% to 150% for CVh. Considering the best model, with the CVr scenario, good prediction accuracies were obtained for glucose (R2 = 0.81), urea (R2 = 0.73), albumin (R2 = 0.75), total reactive oxygen metabolites (R2 = 0.79), total thiol groups (R2 = 0.76), ceruloplasmin (R2 = 0.74), total proteins (R2 = 0.81), globulins (R2 = 0.87), and Na (R2 = 0.72). Good prediction accuracy in classifying extreme values was achieved for glucose (Q25 = 70.8%, Q75 = 69.9%), albumin (Q25 = 72.3%), total reactive oxygen metabolites (Q25 = 75.1%, Q75 = 74%), thiol groups (Q75 = 70.4%), total proteins (Q25 = 72.4%, Q75 = 77.2.%), globulins (Q25 = 74.8%, Q75 = 81.5%), and haptoglobin (Q75 = 74.4%). In conclusion, our study shows that FTIR spectra can be used to predict blood metabolites with relatively good accuracy, depending on trait, and are a promising tool for large-scale monitoring.

Changes in the parameters of pro-oxidant–antioxidant balance in the brain of rats with stepwise incomplete cerebral ischemia

Objective: to evaluate the activity of oxidative stress in rats with stepwise incomplete cerebral ischemia (SICI). Material and methods. Experiments were performed on 24 male outbred rats weighing 260±20 g, allocated into 3 subgroups (6 animals in each) based on time of ligation of both common carotid arteries (CCA). The control group comprised of sham-operated rats of the same sex and similar weights (n=6). To identify the pro-oxidant–antioxidant state of the brain based on its homogenates, the activity of lipid peroxidation processes, the content of thiobarbituric acid reactive substances (TBARS), the concentration of reduced glutathione (GSH), total thiol groups (TSH), and the activity of glutathione peroxidase were determined. Results. SICI with ligation interval of both CCAs of 1 day and 3 days led to a significant decrease in the total SH groups of proteins and glutathione by 30% (p=0.038) and 46% (p=0.044), respectively, TBARS concentration by 29% (p=0.038) and 31% (p=0.043), respectively. SICI with the maximum interval between CCA ligations was manifested by less pronounced changes in the pro-oxidant–antioxidant state of the brain. Conclusion. In SICI with ligation of both CCAs 7 days apart, at which histological changes were the least pronounced, changes in the pro-oxidant–antioxidant balance were insignificant. The most pronounced disorders of the pro-oxidant–antioxidant balance in the brain were observed in the subgroup with the minimum interval between CCA ligations, which implied the highest activity of oxidative stress.