Oxidative stress

The current work aimed at studying the impact of royal jelly on kidney damage caused by rhabdomyolysis in male rats.

40 male rats were randomly assigned to five groups of eight: control, rhabdomyolysis, and rhabdomyolysis, administered with three doses of royal jelly (RJ) (100, 200, and 400 mg/kg) for seven days. On the fifth day, we injected glycerol intramuscularly to induce rhabdomyolysis. Researchers examined serum biochemical parameters, inflammation, oxidative stress, apoptosis, and kidney tissue injury.

As a result of injecting glycerol, serum levels of creatinine, urea, and creatine phosphokinase were considerably elevated. The concentration of inflammatory mediators, as well as the expression of apoptotic parameters, was significantly elevated after glycerol injection. The percentage of kidney tissue damage and neutrophil gelatinase-associated lipocalin expression also increased significantly. Oral usage of RJ (100, 200, and 400 mg/kg) caused a decline in serum CPK, tissue level of total thiols, catalase activity, and renal expression of   BAX compared to the rhabdomyolysis group. Serum creatinine and NGAL expression were also significantly reduced by the RJ (200 and 400 mg/kg). RJ significantly reduced the concentration of inflammatory mediators at 100 and 200 mg/kg doses and the expression of bcl2 by RJ at 100 and 400 mg/kg doses.  

Royal jelly safeguards the kidney from rhabdomyolysis-related damage, primarily through its anti-oxidant, anti-apoptotic, and anti-inflammatory effects.

Cyclophosphamide (CP) is a chemotherapeutic drug used to treat various tumors. It causes nephrotoxicity by producing reactive oxygen species. Sinapic acid (SA) exhibits anti-oxidant, antiapoptotic, and anti-inflammatory activities at low doses as a phenylpropanoid. This study aimed to investigate the protective effects of SA on SP-induced renal injury. 

Forty-eight BALB/c mice were randomly divided into control, SA (for seven consecutive days, with two doses of 5 and 10 mg/kg), CP (single dose, 200 mg/kg), and CP + SA (5 and 10 mg/kg). On the 10th day of the study, mice were examined by renal function markers (Urea and Creatinine), oxidative stress markers (MDA and GSH), histopathological, and immunohistochemical assays (caspase-3 and NF-kB kidney). 

MDA levels increased and GSH levels decreased significantly in CP-treated mice. In addition, the histopathological structure of the kidney tissue in CP-treated mice showed significantly severe kidney tissue damage associated with increased urea and creatinine. The administration of SA in CP-treated mice significantly reduced serum urea and creatinine concentrations. In addition, the immunohistochemical staining of caspase- 3 and NF-kB decreased significantly in the CP + SA group compared to CP-treated mice. 

Overall, our study suggests that sinapic acid, a substance with antioxidant, antiapoptotic, and anti-inflammatory properties, can be used as a complementary therapy to protect nephrotoxicity against CP.

Polycystic ovarian syndrome (PCOS) is a prevalent hormonal disorder among women of reproductive age, resulting in female infertility. Researchers are exploring safe and affordable treatments for this disorder.

This study explored the therapeutic effects of fennel essential oil (FEO) and manganese (Mn) on hormonal and histological markers in rats with estradiol valerate-induced PCOS.

In this experimental study, 35 adult female Wistar rats (9 wk old, 200-250 gr) were divided into 7 groups. For 14 days, groups 1-4 received normal saline intraperitoneally, sesame oil intramuscularly, FEO intraperitoneally, and Mn orally, respectively. PCOS was induced in remaining groups through a single intramuscular injection of estradiol valerate. 60 days after induction, the 6th and 7th groups were treated individually with intraperitoneal FEO and oral Mn for 14 days. Blood samples were analyzed for estrogen, progesterone, and malondialdehyde (MDA) markers. The ovarian tissues were histologically examined to assess cyst formation and structural changes.

FEO significantly increased estrogen and progesterone levels in PCOS rats compared to the PCOS group (p ≤ 0.05). Mn also elevated progesterone levels, but the change was not statistically significant (p > 0.05). No significant differences in MDA levels were observed between the PCOS and PCOS+FEO groups. Although MDA levels decreased in the PCOS+Mn group, the reduction was not statistically significant (p > 0.05). Both FEO and Mn treatments significantly reduced ovarian cyst numbers compared to untreated PCOS rats (p ≤ 0.05).

FEO and Mn demonstrated potential in restoring hormonal balance and improving ovarian histology, offering promise as low-cost treatments for PCOS.

This article has been extracted from Pharm. D. Thesis. (Ensiyeh Mohebbi Kian)

Bisphenols (BP) are endocrine-disrupting chemicals that cause adverse health effects, including testicular steroidogenesis disturbance. Cyclo-oxygenase-2 and nuclear factor erythroid 2-related factor 2 are the target molecules involved in testicular steroidogenesis disturbance via inflammation and oxidative stress (OS), respectively. Interestingly, endoplasmic reticulum (ER) stress was found to be involved in various pathological conditions. However, the mechanisms involved in BP-induced testicular steroidogenesis disturbance remain unclear. Therefore, this research investigates the key mechanisms underlying BP-induced testicular steroidogenesis disturbances. We focus on 3 critical pathways: inflammation, OS, and ER stress. Our findings demonstrate that BP exposure triggers inflammatory responses by targeting the cyclo-oxygenase-2 molecules that impair Leydig cell function. Concurrently, we observed that BP-increased OS via inhibition of nuclear factor erythroid 2-related factor 2, further disrupting steroidogenic enzyme activity. Additionally, ER stress is activated in response to BP exposure, leading to impaired protein synthesis and exacerbating steroidogenic dysfunction. This review elucidates the interlinkage between inflammation, OS, and ER stress in BP-induced testicular steroidogenesis disturbance in which reactive oxygen species is proposed to be the main culprit in linking these 3 mechanisms. These insights provide a crucial foundation for understanding the reproductive toxicology of BPs and inform future strategies for mitigating their effects on male reproductive health.

The utilization of amorphous silica nanoparticles (SiNPs) is gaining popularity in various applications, but it poses a potential risk to human and environmental health. However, the underlying causes and mechanisms of SiNPs-induced kidney damage are still largely unknown.

This study aimed to investigate the SiNPs-induced damage in the kidney and further explore the possible mechanisms of SiNPs-induced nephrotoxicity.

Thirty adult male rats were divided into 3 different groups. Rats in groups 2 and 3 were administered SiNPs at 2 dosage levels (25 and 100 mg/kg of body weight), while the rats in the control group received no treatment for 28 days. Reactive oxygen species (ROS), antioxidant enzyme activities (glutathione peroxidase [GPx], superoxide dismutase [SOD], and catalase [CAT]), glutathione (GSH) levels, and oxidation markers (such as lipid peroxidation [malondialdehyde (MDA)] and protein oxidation [protein carbonyl (PCO)]) were analyzed in the kidney tissue. Additionally, renal fibrogenesis was studied through histopathological examination and the expression levels of fibrotic biomarkers.

The findings revealed that in vivo treatment with SiNPs significantly triggered oxidative stress in kidney tissues in a dose-dependent manner. This was characterized by increased production of ROS, elevated levels of MDA, PCO, and nitric oxide (NO), along with a significant decline in the activities of SOD, CAT, GPx, and reduced GSH. These changes were consistent with the histopathological analysis, which indicated interstitial fibrosis with mononuclear inflammatory cell aggregation, tubular degeneration, glomerulonephritis, and glomerular atrophy. The fibrosis index was confirmed using Masson’s trichrome staining. Additionally, there was a significant upregulation of fibrosis-related genes, including transforming growth factor-beta 1 (TGF-B1), matrix metalloproteinases 2 and 9 (MMP-2/9), whereas the expression of tissue inhibitor of metalloproteinase 2 (TIMP2) was downregulated.

This study provided a new research clue for the role of ROS and deregulated TGF-B signaling pathway in SiNPs nephrotoxicity.

Polycystic ovary syndrome (PCOS) is the most common gynecological endocrine disorder.

This study evaluated the therapeutic effects of Pimpinella anisum L. (P. anisum) fruit on pro-inflammatory cytokines, oxidative stress markers, and ovarian tissue structure in a rat model of PCOS.

After inducing PCOS, female Wistar rats were randomly divided into control and PCOS groups. They orally received daily doses of normal saline or hydro-alcoholic extract of P. anisum at two doses (200 and 400 mg/kg) for 21 days. At the end of the treatment period, ovarian and liver tissues were collected to measure lipid peroxidation, antioxidant status, TNF-, IL-6 mRNA expression, and its content. Additionally, histopathological examinations of the ovarian tissue were conducted.

Our findings revealed a dose-dependent change in the biochemical and histopathological parameters. Treatment with P. anisum resulted in a significant decrease in TNF-and IL-6mRNAexpression levels and their content in the ovarian and liver tissues. It also reduced MDA levels while increasing SOD and GPx activity in both ovarian and liver tissues of PCOS rats. Furthermore, the number of follicular cysts in the PCOS rat model was significantly reduced.

The beneficial effects of P. anisum in PCOS rats are partly attributed to the inhibition of inflammatory and oxidative stress markers in ovarian tissue. These findings suggest that P. anisum could be a potential candidate for the treatment of PCOS disorders

Doxorubicin (DOX) is used in the treatment of various cancers and has good effectiveness. However, its therapeutic use is limited due to its effects on various organs and healthy cells. Doxorubicin can affect the kidneys and cause toxicity. Evidence shows that DOX induces nephrotoxicity through oxidative stress.

In this research, we examined the effect of mitochondrial transplantation on improving mitochondrial and cellular toxicity caused by DOX on renal proximal tubular cells (RPTCs).

The research measured 7 toxicity parameters, including cell lysis, reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP) decline, GSH and GSSG content, lipid peroxidation (LPO), adenosine triphosphate (ATP) content, and Caspase-3 activity (the final mediator of apoptosis). Active fresh mitochondria were prepared from Wistar rat kidney.

The findings indicated that DOX caused cytotoxicity in RPTCs. Additionally, DOX induced oxidative stress by increasing the level of reactive oxygen species, reducing glutathione content, and elevating lipid peroxidation. Moreover, it led to damage to the mitochondrial membrane, increased caspase-3 activity, and decreased ATP content. Mitochondrial transplantation, as a new therapeutic approach, reduced oxidative stress, mitochondrial membrane damage, and apoptosis caused by DOX in RPTCs. Furthermore, this therapeutic approach increased the ATP content in RPTCs.

Our study suggests that this therapeutic approach could be helpful in the treatment of drug-induced nephrotoxicity.

This study aims to investigate the effects of sodium hydrogen sulphide (NaHS) supplementation, a hydrogensulphide (H2S) donor, on oxidant and antioxidant markers, as well as sperm function in rats with experimentally inducedvaricocele.

In this experimental study, 55 male Wistar rats were assigned to varicocele (n=25), control (n=20),and sham (n=10) groups. In the varicocele group, five rats received NaHS treatment immediately after surgery for fourmonths and ten rats were treated two to four months after surgery. The remaining ten rats in the varicocele group receivedno treatment. Similar protocols were followed for the control groups. At the end of four months, all rats were sacrificed, andassessments were made for sperm parameters that included function tests, and testicular malondialdehyde (MDA) and totalantioxidant capacity (TAC).

Varicocele induction significantly impaired sperm parameters and sperm function tests. NaHS treatment fortwo months increased sperm concentrations, while treatment for two and four months improved motility, chromatinstatus, and intracellular reactive oxygen species (ROS) compared to untreated varicocele rats. After four months, NaHStreatment reduced testicular MDA levels. Testicular TAC significantly increased after two months but decreased afterfour months of treatment in the varicocele group (P<0.05).

NaHS treatment improved sperm parameters and reduced oxidative stress in varicocele rats. Theobserved effects depended on the treatment duration.

High glucose (HG)-induced oxidative stress is a metabolic stimulus for hepatic impairment in diabetes. Naturalphytochemicals may alleviate HG-induced complications. We aimed to examine the impact of citronellol (CT) on oxidativestress and inflammation in the human hepatocellular liver carcinoma (HepG2) cell line under HG conditions. In this experimental study, the HepG2 cells were exposed to HG concentrations of 50 mM andco-treated with or without CT at concentrations of 10, 20, and 40 μg/ml for 48 hours. The impact of treatments on the levelsof malondialdehyde (MDA), glutathione (GSH), and the enzyme’s activity of glutathione peroxidase (GPx), catalase (CAT),and superoxide dismutase (SOD) was explored. We used quantitative reverse transcription polymerase chain reaction (qRTPCR)to evaluate the gene expression of nuclear factor-κβ (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6),and dipeptidyl peptidase-4 (DPP-4). Co-treatment with CT (20 and 40 μg/ml) significantly reduced (P<0.05) HG-induced cell death (9.73 and10.56%, respectively) and MDA production (16 and 26.78%, respectively) compared to untreated HG control group.Meanwhile, CT (10, 20, and 40 μg/ml) substantially increased (P<0.05) GSH content (35.61, 55.24, and 69.75%,respectively), GPx (48.32, 61.75, and 75.10%, respectively), and CAT activity (20.25, 25.09, 30.16%, respectively)dose-dependently comparison to untreated ones. TNF-α and IL-6 gene expression were also modulated significantly(P<0.05) by 40 μg/ml CT (47.75 and 32.44%, respectively) as compared to the HG control group. Moreover, CT at 20and 40 μg/ml attenuated (P<0.05) NF-κB gene expression (30.41 and 39.93%, respectively), and at all doses, made aconsiderable reduction (P<0.05) in DPP-4 gene expression (18.77, 18.78, and 44.61%, respectively) dose-dependentlycomparison to untreated ones. Our research suggested that CT with greater effectiveness at 40 μg/ml might shield hepatocytes exposedto HG by lowering oxidative stress and inhibiting inflammatory reactions; however, more research is needed.

In our study, the neuroprotective efficacy of pre- and post-traumatic applications of boric acid (BA) in rats with experimentally induced spinal cord injury (SCI) was investigated.

The experimental animals were divided into four groups: control group (C), SCI group (SCI), BA-treated group before SCI (BA+SCI), and BA-treated group after SCI (SCI+BA). Forty-eight hours after SCI, biochemical levels of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and cytochrome c (Cytc) and caspase-3 (Casp3) expressions were measured in the spinal cord tissues and were examined histologically.

After SCI, oxidative stress markers, such as MDA, TOS, and OSI, and apoptosis markers Cytc and Casp3 showed an increase in levels compared to Group C. The oxidative stress markers that increased after SCI decreased with BA+SCI application, while Cytc level, one of the apoptosis markers that increased after SCI, decreased in both groups with BA application. Cell, myelin, ependymal damage, and hemorrhage levels increased after SCI compared to Group C. These histological markers increased after SCI and decreased after BA+SCI. BA was found to reduce SCI-induced oxidative stress and oxidative stress-induced apoptosis.

BA administered before SCI was shown to be more effective in protecting neural damage.

Diclofenac (Diclo) is a therapeutic agent used in the treatment of pain and inflammatory diseases, but it is also toxic to the human body. Morin is a flavonoid found naturally in plants and has many biological and pharmacological activities, including anti-inflammatory, anti-oxidant, and anticancer activities. This study aimed to investigate the efficacy of Morin in Diclo-induced testicular toxicity. 

Morin (50 mg/kg and 100 mg/kg) was administered orally for five days, while Diclo was administered intraperitoneally at 50 mg/kg on days 4 and 5. Biochemical, molecular, and histological methods were used to investigate oxidative stress, inflammation, apoptosis, and endoplasmic reticulum (ER) stress damage indicators in testicular tissue. 

Morin treatment attenuated Diclo-induced oxidative stress damage by increasing anti-oxidant levels (SOD, CAT, GPx, GSH, Nrf-2, HO-1, and NQO1) and decreasing MDA levels, an indicator of lipid peroxidation. Morin reduced levels of the inflammatory mediators NF-κB protein. Increases in apoptotic Bax and Caspase-3 by Diclo were reduced by Morin, while decreased antiapoptotic Bcl-2 level was increased. Morin reduced Diclo-induced ER stress injury by decreasing ATF-6, PERK, IRE1, GRP-78, and CHOP levels. Also, Diclo decreased COX-2 levels.

Overall, Morin may be an effective treatment of choice for testicular tissue damage associated with Diclo toxicity and may reduce the level of damage.

Platelet-rich plasma (PRP) contains multiple growth hormones that may stimulate tissue repair. We aimed to assess PRP’s efficacy and explore possible mechanisms using the intervertebral disc degeneration (IDD) model. 

A total of 48 male Sprague-Dawley (SD) rats were randomly divided into three groups: sham, IDD+PBS, and IDD+PRP (n=16, respectively). IL-1β (10 ng/ml) was used to establish a humanized IDD model in human lumbar nucleus pulposus (NP) tissues from 36 patients with degenerative disc disease. These NP cells were randomly divided into three groups: sham, IDD+PBS, and IDD+PRP (n=12, respectively). RT-PCR and western blot were used to detect the expression of aggrecan, collagen II, IL-1β, IL-6, TNF-α, Bcl-2, cleaved-Caspase 3, Bax and Akt/mTOR/p70S6K signaling pathway. A related assay kit was used to detect MDA, SOD, and GSH.

PRP affected the expression of aggrecan, collagen II, IL-1β, IL-6, TNF-α, MDA, SOD, GSH, Bcl-2, cleaved-Caspase 3, and Bax in IDD rats. Compared with the IDD+PBS group, the expression of p-mTOR, p-p70/S6K, and p-Akt was much lower in the rat IDD+PRP group (P<0.05). Similarly, with PRP treatment in the humanized IDD model, the expression of p-mTOR, p-p70/S6K, and p-Akt was also inhibited.

PRP may be a potential therapy for IDD via the mTOR signaling pathway in regulating and affecting extracellular matrix degradation, inflammatory factors, oxidative stress, and apoptosis.

The present study investigated the protective effect of melittin (MEL) against bleomycin (BLM)- induced pulmonary fibrosis (PF) in mice and the mechanism underlying this effect.

A mouse model of PF was established by intratracheal injection of 3.5 mg/kg BLM. Twenty-four hours after the model was established, the mice in the treatment groups were intraperitoneally injected with MEL, and specimens were collected 28 days later. The body weight, survival rate, and pulmonary index (PI) of the mice were determined. Haematoxylin and eosin (HE) staining, Masson’s trichrome staining, immunohistochemical staining, kit assays, and Western blot (WB) analysis were performed.

Our study indicated that MEL significantly increased the body weight and survival rate, reduced PI, and improved lung histopathology in mice. In addition, MEL inhibited epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) deposition. Attenuated mitochondrial damage and reduced oxidative stress (OS) were also observed in MEL-treated mice. We further showed that MEL inhibited the TGF-β1/Smad2/3 pathway and activated the AMPK/SIRT1/PGC-1α pathway.

MEL is a promising future therapeutic agent for PF. Its multifaceted and complex mechanism of action inhibits both EMT and ECM production by modulating the TGF-β1/Smad2/3 pathway. It also improves mitochondrial function and reduces OS at least partially through the activation of the AMPK/SIRT1/PGC-1α signaling pathway.

Non-alcoholic fatty liver disease (NAFLD) is a general term encompassing many conditions from simple fatty liver to cirrhosis and hepatocellular carcinoma. In this research, we aimed to investigate the effect of the antioxidant protocatechuic acid (PCA) in preventing the development of fatty liver induced by high-fat diet (HFD) in male mice.

Mice (NMRI) were randomly divided into five groups. The groups were as follows: the control received the standard diet, HFD received 20 ml/kg of HFD, HFD containing PCA received HFD containing 200 mg/kg/20 ml of PCA, HFD containing fenofibrate (FENO) received HFD containing 150 mg/kg/20 ml of FENO, and PCA received 200 mg/kg/20 ml of PCA alone for six weeks. Mice were anesthetized after overnight fasting on the 43rd day, and the blood sample was collected from their hearts. The levels of serum, antioxidants and pro-inflammatory factors were measured, and histological studies were performed.

The results showed that HFD containing PCA decreased liver enzymes, cholesterol (Chol), and thiobarbituric acid reactive substances (TBARS) levels and increased high-density lipoprotein (HDL), and total thiol levels in the liver compared to the HFD group alone (P<0.001). The histopathological examinations of the liver tissue confirmed the biochemical results. High-fat diet (HFD) containing PCA showed no significant effect on the levels of triglyceride (TG), low-density lipoprotein (LDL), catalase, and superoxide dismutase (SOD). The histopathological examinations of the liver tissue confirmed the biochemical results.

The findings of this study demonstrated that PCA is reasonably effective in preventing NAFLD in mice.

Acetaminophen also name paracetamol is apopular antipyretic and analgesic drug, in alarge doses produces a cute kidney injury either in human and animals. The aim of this study to assess the effect of celastrol in reducing acetaminophen-induced nephrotoxicity and to elucidate its underlying mechanisms.

Rats were divided into four groups: control, celastrol-treated, acetaminophen-exposed, and a group receiving both acetaminophen and celastrol. After 24 hours, blood samples were taken and kidney tissues were harvested for histological and molecular analyses. The findings shed light on the protective effects of celastrol against acetaminophen-induced nephrotoxicity, offering insights into its therapeutic potential.

paracetamol oral intake altered renal histology with significantly P< 0.05 increased serum creatinine, blood urea nitrogen (BUN), and homogenate malonaldhyde (MDA), and immunoexpression of tumor necrosis- alpha (TNF-α), interleukin-6 (IL-6), caspase-3, Bcl-2-associated X- protein (Bax). Furthermore, it decreases homogenate level of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and gene expression of nuclear factor erythroid 2–related factor 2 (Nrf2), and haem oxygenase-1 (HO-1). Meanwhile, intraperitoneal injection of celastrol with acetaminophen reaffirms the previous results.

We provided a novel treatment against acetaminophen induced-nephrotoxicity with targeting renal oxidative stress, inflammation, apoptosis with elevation of Aquaporin 1 (AQP1) level.

SARS-CoV-2 infection can cause significant alterations in our lives. Oxidative stress (OS) has been proposed to play a major role in COVID-19 pathogenesis, and the determination of OS biomarkers provides insight into disease severity.

The study was conducted during the second wave of the pandemic in 2020. Fifty blood samples were collected from patients admitted to one of the COVID-19 isolation centers in Baghdad, Iraq. The samples were subdivided into 25 patients admitted to the intensive care unit (ICU) and 25 non-ICU patients, compared to 25 healthy controls. All participants were aged 35-52 years.

The study showed that the mean (±SD) serum total oxidant status (TOS) and malondialdehyde (MDA) levels were significantly increased (p< 0.001) in the ICU group compared to the control and non-ICU groups. Conversely, the levels of serum total antioxidant capacity (TAC) and serum antioxidative enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase, and glutathione (GSH) were significantly decreased (p< 0.001) in the ICU group compared to both the control and non-ICU groups. Serum zinc levels were significantly decreased (p< 0.001) in both ICU and non-ICU groups compared to the control group, while serum selenium (Se), copper (Cu), and vitamins C and E were significantly decreased (p< 0.001) in the ICU group compared to both the control and non-ICU groups.

The presence of OS biomarkers in the sera of COVID-19 patients offers a potential new approach for the treatment of this disease.

The objective of this study was to compare the effects of early time?restricted eating (eTRE) and eTRE plus probiotic supplementation to daily caloric restriction (DCR) alone in terms of biomarkers of oxidative stress (OS), antioxidant capacity, inflammation, and blood pressure (BP) in obese women with polycystic ovary syndrome (PCOS).

The research was conducted as a randomized, parallel, placebo?controlled clinical trial with an 8?week follow?up period. Participants were randomly assigned to one of three groups: 14:10 eTRE with probiotic supplementation (n = 30), 14:10 eTRE with placebo supplementation (n = 30),or DCR with placebo supplementation (n = 30). At the beginning and 8 weeks of the intervention, systolic blood pressure (SBP) and diastolic BP, inflammation, and OS parameters were evaluated.

A total of 90 participants (mean age, 30.49 years and mean weight, 81.45 kg) were enrolled in this trial. After 8?week intervention, we observed SBP significantly decreased in both the eTRE + probiotic group (?0.31 mmHg [95% confidence interval (CI): ?0.55, ?0.07]) and the eTRE + placebo group (?0.24 mmHg [95% CI: ?0.43, 0.04]), with no significant differences observed between groups. Moreover, C?reactive protein (CRP) levels were significantly reduced in all groups (P < 0.005). Total antioxidant capacity (TAC) also showed notable improvement in both the eTRE + probiotic group (P = 0.012) and the DCR group (P = 0.032). However, there were no significant differences between the three groups regarding BP, OS, TAC, and CRP markers.

It was not found that eTRE alone or eTRE with probiotics intervention resulted in improving BP, inflammatory, OS, and antioxidant capacity biomarkers than a standard DCR diet among obese women with PCOS. The present study did not reveal significant improvements in BP, inflammatory markers, OS, or antioxidant capacity with either eTRE alone or eTRE combined with probiotics compared to a standard DCR among obese women diagnosed with PCOS.Trial Register no: IRCT20121110011421N5.

Nonalcoholic fatty liver disease (NAFLD) is known to disrupt testicular anti-oxidant capacity, leading to oxidative stress (OS) that can negatively affect male fertility by damaging sperm DNA. Heat shock proteins (HSP70 and HSP90), in association with transitional proteins (TP1 and TP2), play crucial roles in protecting sperm DNA integrity in oxidative conditions. Whiteleg shrimp protein hydrolysates (HPs) exhibit anti-oxidant properties, prompting this study to explore the potential of HPs in ameliorating NAFLD-induced testicular damage. 

The study divided rats into four groups: control, a group subjected to a high-fat diet (HFD) to induce NAFLD without supplementation, and two HFD-induced NAFLD groups receiving HP doses (20 and 300 mg/kg). After 70 days, the testicular total anti-oxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), HSP70-2a, HSP90 expression, and TP mRNA levels were assessed. 

The results showed that HFD-induced NAFLD significantly increased GSH and MDA levels and disrupted the GSH/GSSG ratio (P<0.05) while also reducing HSP70-2a, HSP90, TP1, and TP2 expression (P<0.05). However, HP administration effectively restored testicular redox balance, reduced oxidative stress, and enhanced these protective proteins’ expression compared to HFD (P<0.05). 

NAFLD negatively affects the testicular redox system and HSP and TP expression, disrupting male fertility potential. In contrast, HP-treated rats showed a marked effect on NAFLD-induced damage by improving testicular anti-oxidant status and regulating the expression of HSPs and TP proteins. These findings suggest a potential therapeutic role for HP in safeguarding male fertility against the damaging effects of NAFLD.

Exposure to sodium fluoride (Naf) via sources such as the environment, use of toothpaste, pesticides cause toxicity in the liver, kidney and brain where it induces oxidative stress. Vitamin B plays an important role in the body by taking part in metabolism and scavenging of free radicals thereby protecting the body against oxidative stress. Therefore, the aim of this research was to determine the ameliorative effect of vitamin B on sodium fluoride induced hepato-renal and brain damage.

 Twenty (20) adult male Wistar rats were used for the experiment. They were randomly divided into four groups of five rats each; Group I were administered distilled water, Group II NaF at 600ppm, Group III NaF at 600ppm + Vitamin B (10 ml/kg/day) and group IV Vitamin B (10 ml/kg/day) administered orally, daily for four weeks. Hematology, serum biochemical and oxidative stress markers in the liver, kidney and brain were analyzed.

WBC, RBC, PCV and hemoglobin were decreased in the NaF group. Also, serum ALT, AST, ALP, urea and creatinine were significantly (p<0.05) increased. There was significant decrease (p<0.05) in the liver, kidney and brain catalase, glutathione peroxidase and superoxide dismutase. There was significant increase (p<0.05) in liver, kidney and brain malondialdehyde in NaF group compared to other groups.

Administration of Vitamin B alone did not cause any biochemical alterations in the liver, kidney and brain. Co-administration of NaF and Vitamin B for four weeks ameliorated the oxidative changes induced by NaF in the liver, kidney and brain