Food deprivation and social inequality may lead to oxidative damage: a study on the preventive role of melatonin in the male rat reproductive system

2016 ◽  
Vol 28 (8) ◽  
pp. 1232
Author(s):  
Shiva Nasiraei-Moghadam ◽  
Kazem Parivar ◽  
Abolhasan Ahmadiani ◽  
Mansoureh Movahhedin ◽  
Mohammad-Reza Vaez Mahdavi

Spermatogenic cells are susceptible to oxidative stress and apoptosis. Food deprivation (FD) has been reported as a stressor that could increase reactive oxygen species. In the present study, FD-induced oxidative stress and apoptosis, as well as the protective effects of melatonin, were evaluated in the testes. Wistar rats in the control group were fed a standard diet, whereas a sham group was administered saline as the melatonin vehicle. A third group received daily injections of melatonin (5 mg kg–1 bodyweight). These rats were further divided into four groups of rats that were either subjected to FD, FD + isolation, FD + melatonin injection and FD + melatonin injection + isolation. Testicular tissues were evaluated for malondialdehyde (MDA) and reduced glutathione (GSH) concentrations, as well as and DNA damage. FD increased MDA and reduced GSH concentrations, whereas melatonin treatment improved these parameters. Immunohistochemistry for capsase-3 and terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling revealed that the number of apoptotic cells was increased in rats subjected to FD alone. Melatonin treatment offset the number of apoptotic cells following FD. The results provide evidence that FD can increase oxidative stress, leading to activation of apoptosis, and that melatonin has the ability to protect the testes against oxidative damage induced by FD.

2020 ◽  
Vol 17 (3) ◽  
pp. 191-199
Author(s):  
Seval Yilmaz ◽  
Fatih Mehmet Kandemir ◽  
Emre Kaya ◽  
Mustafa Ozkaraca

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.


Author(s):  
Akinleye Stephen Akinrinde ◽  
Halimot Olawalarami Hameed

Abstract Objectives This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (l-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), l-Arg1 (200 mg/kg) and l-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematological, biochemical and histopathological analyses were then carried out. Results DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and l-Arg resulted in significant amelioration of the DIC-induced alterations although l-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions The data from this study suggest that Gly or l-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.


Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.


2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.


PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0250885
Author(s):  
Zhaofang Chen ◽  
Kexin Shi ◽  
Wenjie Kuang ◽  
Lei Huang

Cadmium (Cd) is a toxic non-essential element, while calcium (Ca) is an essential element with high chemical similarity to Cd. Dietary intake is the major Cd exposure pathway for non-smokers. A multi-concentration dietary intervention experiment was designed to explore the optimum concentration of Ca in diet with obvious protective effects against the toxicity of livers and kidneys induced by Cd in mice. The mice were divided into six groups with different concentrations of Cd and Ca in their food: control-group (no Cd or Ca), Ca-group (100 g/kg Ca, without Cd), Cd-group (2 mg/kg Cd, without Ca), CaL+Cd-group (2 mg/kg Cd, 2 g/kg Ca), CaM+Cd-group (2 mg/kg Cd, 20 g/kg Ca) and CaH+Cd-group (2 mg/kg Cd, 100 g/kg Ca). The organ indexes, oxidative stress biomarkers, lesions and Cd concentrations were detected after a 30-day exposure period. Results showed that serum Aspartate Aminotransferase (AST) level in CaH+Cd-group was significantly lower than that in Cd-group, while close to that in control-group. The contents of Serum Blood Urea Nitrogen (BUN) in different groups showed the same trend. Concentrations of all oxidative stress biomarkers (GSH-Px, SOD, CAT, GSH and MDA) in CaH+Cd-group were close to the normal levels of control-group while significantly different from those in Cd-group. The only exception was the Malondialdehyde (MDA) levels in kidneys. This study suggests that Ca plays a protective role in relieving the Cd-induced toxicity of livers and kidneys and a concentration of 100 g/kg for Ca in diet showed the best protective effects. These findings could provide a clue for further studies concerning human diet intervention for Cd control.


2021 ◽  
Vol 68 (1) ◽  
pp. 222-228
Author(s):  
Ahmet Özkaya ◽  
Kenan Türkan

In this study, the effects of 3-benzoyl-7-hydroxy coumarin molecule on mineral and antioxidant enzymes were investigated in rat liver exposed to oxidative stress with aluminium chloride (AlCl3). Adult male Wistar albino rats were divided into four groups as Control, Coumarin, AlCl3, and Coumarin + AlCl3. Coumarin at the dose of 10 mg/kg and AlCl3 at the dose of 8.3 mg/kg were administered for 30 days every other day. In AlCl3 group, malondialdehyde (MDA), iron (Fe), aluminium (Al) and copper (Cu) levels increased compared to the control group, while glutathione (GSH) level, glutathione S-transferase (GST), and carboxylesterase (Ces) enzyme activity levels decreased. In Coumarin + AlCl3 group, MDA, Fe, Al and Cu levels decreased with the effect of coumarin compared to AlCl3 group, while GSH level, and GST enzyme activity levels increased. According to our results, AlCl3 generates oxidative stress in rat livers, and we believe that 3-benzoyl-7-hydroxy coumarin has an ameliorative effect on antioxidant enzyme system, Al, Fe and Cu levels.


2021 ◽  
Vol 12 (2) ◽  
pp. 1762-1777

Doxorubicin (DOX) is effective chemotherapy in several malignancies, but large-scale toxicities limit its clinical usefulness. Propolis has been reported to exhibit a broad spectrum of biological activities. We aim to assess the protective efficacy of propolis against DOX-induced multi-toxicity in female rats. Forty female rats were divided into four groups: control group; Group (P) were administrated oral propolis (100 mg/kg once daily for 28 days); Group (P+DOX) were injected with a single intraperitoneal dose of DOX (20 mg/kg i.p at 24th day after the propolis administration) and group (DOX) were injected with doxorubicin only. Estimation of cardiac, renal and hepatic injury markers, apoptosis and pro-inflammatory cytokines were done using sera. Also, liver and heart tissue samples were collected to determine GSH and MDA as oxidative stress markers. In addition to histopathological and immunohistochemical examination of Cytochrome-C and Connexin43 on lysed myocardium, liver, kidney and lung tissues. Doxorubicin toxicity caused marked deteriorations of measured parameters through the different mechanisms in different body organs. However, pre-treatment with propolis significantly ameliorated these alterations. Thus propolis can ameliorate the DOX-induced experimental multi-toxicity as cardiomyopathy, hepatotoxicity, nephritis and pneumonia. Thus, it could be a promising protective agent in DOX treatment protocols.


2021 ◽  
Vol 15 (9) ◽  
pp. 2952-2954
Author(s):  
Roomisa Anis ◽  
Misbah-ul- Qamar ◽  
Ayesha Shafqat ◽  
Ayesha Aftab ◽  
Zarafshan Bader ◽  
...  

Lead (Pb) is an abundant and one of the most lethal metals found in the earth’s crust. Its use by humans dates back to thousands of year. Even the low doses of lead are responsible for the production of reactive oxygen species which leads to oxidative load. This oxidative stress mitigates production of malondialdehyde (MDA) and down regulates antioxidant enzyme superoxide dismutase (SOD). Study Design: Quasi experimental Study. Place and duration of study: Department of Biochemistry, ANMCH, Islamabad, Pakistan in collaboration with NIH, Islamabad from November, 2018 to April, 2019. Methodology: A total of 40 BALB/c mice were divided into two groups of 20 mice each. Group  was given normal standard diet. Group  was given lead acetate in drinking water with normal diet without any supplementation. Levels of malondialdehyde were measured by using Thiobarbituric acid reactive substances (TBARS) and Superoxide Dismutase (SOD) was estimated by xanthine oxidase method at the end of study. Results: The results of our study showed increase in MDA and decrease in SOD in lead treated group when compared with the control group. Pearson correlation was applied to assess the degree of association between two parameters, it showed significant negative correlation with value of r = -0.96 and p-value of 0.001 Conclusion: It was concluded from our study that increase in MDA leads to decrease in SOD indicating strong negative correlation in lead poisoned mice. Key words: Lead poisoning, Malondialdehyde, Oxidative Stress, Superoxide Dismutase


2019 ◽  
Vol 8 (5) ◽  
pp. 741-753 ◽  
Author(s):  
Israa F. Mosa ◽  
Mokhtar I. Yousef ◽  
Maher Kamel ◽  
Osama F. Mosa ◽  
Yasser Helmy

Abstract Hydroxyapatite nanoparticles (HAP-NPs) are an inorganic component of natural bone and are mainly used in the tissue engineering field due to their bioactivity, osteoconductivity, biocompatibility, non-inflammatory, and non-toxicity properties. However, the current toxicity data for HAP-NPs regarding human health are limited, and only a few results from basic studies have been published. Therefore, the present study was designed to investigate the beneficial role of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in alleviating nephrotoxicity induced by HAP-NPs in male rats. The results showed that HAP-NPs caused a reduction in antioxidant enzymes and induced lipid peroxidation, nitric oxide production and DNA oxidation. Moreover, HAP-NP administration was associated with intense histologic changes in kidney architecture and immunoreactivity to proliferating cell nuclear antigen (PCNA). However, the presence of CsNPs and/or CurNPs along with HAP-NPs reduced the levels of oxidative stress through improving the activities of antioxidant enzymes. Also, the rats administered the nanoparticles showed a moderate improvement in glomerular damage which matched that of the control group and showed mild positive reactions to PCNA–ir in glomeruli and renal tubules in the cortical and medullary portions. These novel insights confirm that the presence of chitosan and curcumin in nanoforms has powerful biological effects with enhanced bioactivity and bioavailability phenomena compared to their microphase counterparts. Also, they were able to ameliorate the nephrotoxicity induced by HAP-NPs.


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