Marker Of Oxidative Damage Research Articles

Effects of aging and long-term physical activity on mitochondrial physiology and redox state of the cortex and cerebellum of female rats.

We investigated the effects of aging and long-term physical activity on markers of mitochondrial function and dynamics in the cortex and cerebellum of female rats. Additionally, we interrogated markers of oxidative damage and antioxidants. Thirty-four female Lewis rats were separated into three groups. A young group (YNG, n=10) was euthanized at 6months of age. Two other groups were aged to 15 months and included a physical activity group (MA-PA, n=12) and a sedentary group (MA-SED, n=12). There were no age effects for any of the variables investigated, except for SOD2 protein levels in the cortex (+6.5%, p=0.012). Long-term physical activity increased mitochondrial complex IV activity in the cortex compared to YNG (+85%, p=0.016) and MA-SED (+82%, p=0.023) and decreased carbonyl levels in the cortex compared to YNG (-12.49%, p=0.034). Our results suggest that the mitochondrial network and redox state of the brain of females may be more resilient to the aging process than initially thought. Further, voluntary wheel running had minimal beneficial effects on brain markers of oxidative damage and mitochondrial physiology.

Alzheimer brains: increased soluble amyloid peptides, but decreased lipid rafts

AbstractBackgroundPET imaging studies of AD patients show progressive increases of fibrillar Aβ‐ amyloid. Because current PET ligands underestimate non‐fibrillar forms, we assayed soluble Aβ in AD and controls. To identify mechanisms responsible for soluble Aβ in AD brains, we examined lipid rafts (LR), where APP is enzymatically processed. Frontal cortex was compared with cerebellum, which has minimal AD pathology.MethodPostmortem samples (N=48) were age‐and sex matched for Braak scores. Soluble Aβ was extracted from homogenates of full thickness frontal cortex by isotonic buffer and mild detergent (RIPA; 1% NP40) and centrifuged (10,000g/1h). Supernates were assayed by dot blots with antibodies for Aβ40 and Aβ42 (Biolegend, San Diego, CA). Aβ was assayed as relative fluorescent units per gm brain. LR fractions were isolated from these same brains by kit (Invent Biotechnologies; LR‐039), validated by ultracentrifugal fractionation.ResultCompared with cognitively normal controls (Braak 0‐1), elevations of soluble Aβ40 and Aβ42 were similar for intermediate and later stage AD (Braak 2‐3 and 4‐6). Clinical grade AD had greater increase of soluble Aβ40 (+400%) than Aβ42 (+50%) (p<0.05). LR raft yield per gram AD frontal cortex was 20% below controls (p<0.05), while cerebellar LR did not differ by Braak score. The composition of LR had a similar pattern, with 35% AD decreases of total protein and cholesterol (p<0.05); cerebellar LR again did not differ by Braak score. However, LR 4‐HNE, a marker of oxidative damage, was similarly increased in AD cortex and AD cerebellum.ConclusionThe extensive overlap of soluble Aβ levels in controls with AD contrasts with the PET findings on fibrillar Aβ. These findings further support fibrillar Aβ as a biomarker for AD treatments and show the need for more detailed postmortem analysis of diverse soluble and insoluble Aβ aggregates in relation to PET. The decreased LR in AD frontal cortex is consistent with its extensive neuronal loss, in contrast to the cerebellum. Further studies will examine LR enzymes of APP processing as a source of the increased soluble Aβ in AD, and subcellular clearance processes, which may be impaired in association with the oxidative damage indicated by increased 4‐HNE.

CHD4 plays a critical role in arsenite-induced oxidative damage in human urothelial carcinoma.

Inorganic arsenic (iAs), a known human carcinogen, induces oxidative DNA damage and epigenetic silencing of tumor suppressor genes related to tumor progression. Chromodomain-helicase-DNA-binding protein 4 (CHD4) is a chromatin remodeling protein that acts on DNA repair and DNA methylation under oxidative damage in malignancies, but the role of CHD4 in arsenical urothelial carcinoma (UC) is unidentified. Our purpose was to observe CHD4-related repair effects on As-stimulated oxidative damage in human UC. The markers of oxidative DNA damage 8-hydroxy-2'-deoxyguanosine (8-OHdG) and CHD4 were investigated by immunohistochemistry in 45 UC tissues from non-blackfoot disease (BFD) areas and BFD areas respectively. The cellular mechanisms of CHD4 involved in the oxidative DNA repair and DNA methylation were evaluated by immunocytochemistry and western blot. The expressions of CHD4 and 8-OHdG were significantly increased in UC patients from the As-exposed areas. The underlying mechanism of CHD4-mediated DNA repair and DNA methylation involved the activation of zinc finger MYND-type containing 8 (ZMYND8) and DNA methyltransferase (DNMTs) in SV-HUC-1, T24 and BFTC-905 cells. These results highlight the potential clinical significance of CHD4 in UCs from BFD areas. The CHD4-mediated oxidative DNA repair and epigenetic DNA methylation in UC cells stimulated by arsenic was revealed. CHD4 might be used as a prognostic indicator in arsenical UC.

Analysis of Markers of Oxidative Damage of Neurons and Neuroinflammation in the Long-Term Period after Gamma Irradiation of a Mouse Head at Different Doses

Analysis of Markers of Oxidative Damage of Neurons and Neuroinflammation in the Long-Term Period after Gamma Irradiation of a Mouse Head at Different Doses

Adrenomedullin Mitigates Doxorubicin-Induced Nephrotoxicity in Rats: Role of Oxidative Stress, Inflammation, Apoptosis, and Pyroptosis.

Doxorubicin (DOX) is an anticancer antibiotic which has various effects in human cancers. It is one of the commonly known causes of drug-induced nephrotoxicity, which results in acute renal injury. Adrenomedullin (ADM), a vasodilator peptide, is widely distributed in many tissues and has potent protective effects. Therefore, the current study aimed to examine the protective potential mechanisms of ADM against DOX-induced nephrotoxicity. A total of 28 male Wistar rats were randomized into four groups: control group, doxorubicin group (15 mg/kg single intraperitoneal injection of DOX), adrenomedullin + doxorubicin group (12 μg/kg/day intraperitoneal injection of ADM) 3 days prior to DOX injection and continuing for 14 days after the model was established, and adrenomedullin group. Kidney function biomarkers, oxidative stress markers, and inflammatory mediators (TNF-α, NLRP3, IL-1β, and IL-18) were assessed. The expressions of gasdermin D and ASC were assessed by real-time PCR. Furthermore, the abundances of caspase-1 (p20), Bcl-2, and Bax immunoreactivity were evaluated. ADM administration improved the biochemical parameters of DOX-induced nephrotoxicity, significantly reduced oxidative damage markers and inflammatory mediators, and suppressed both apoptosis and pyroptosis. These results were confirmed by the histopathological findings and revealed that ADM's antioxidant, anti-inflammatory, anti-apoptotic, and anti-pyroptotic properties may have prospective applications in the amelioration of DOX-induced nephrotoxicity.

Quantifying the influence of urban biotic and abiotic environmental factors on great tit nestling physiology

There is a long history of avian studies investigating the impacts of urbanization. While differences in several life-history traits have been documented, either between urban and rural populations or across generalized urbanization gradients, a detailed understanding of which specific environmental variables cause these phenotypic differences is still lacking. Here, we quantified several local environmental variables coupled to urbanization (air pollution, tree composition, ambient temperature, and artificial light at night [ALAN]) within territories of breeding great tits (Parus major). We linked the environmental variables to physiological measures of the nestlings (circulating fatty acid composition [FA], antioxidant capacity and an oxidative damage marker [malondialdehyde; MDA]), to garner a mechanistic understanding of the impact of urbanization. We found that the antioxidant capacity of nestlings decreased with higher numbers of oak trees and levels of PM2.5 (airborne particulate matter with a diameter < 2.5 μm). Furthermore, the ratio of ω6:ω3 polyunsaturated FAs, important for immune function, was positively correlated with PM2.5 concentration, while being negatively associated with ambient temperature and number of non-native trees in the territory. Body mass and wing length both increased with the number of local oak trees. We also show, through a principal component analysis, that while the environmental variables fall into an urbanization gradient, this gradient is insufficient to explain the observed physiological responses. Therefore, accounting for individual environmental variables in parallel, and thus allowing for interactions between these, is crucial to fully understand the urban ecosystem.

Cross-reactivity between histone demethylase inhibitor valproic acid and DNA methylation in glioblastoma cell lines.

Currently, valproic acid (VPA) is known as an inhibitor of histone deacetylase (epigenetic drug) and is used for the clinical treatment of epileptic events in the course of glioblastoma multiforme (GBM). Which improves the clinical outcome of those patients. We analyzed the level of 5-methylcytosine, a DNA epigenetic modulator, and 8-oxodeoxyguanosine, an cellular oxidative damage marker, affected with VPA administration, alone and in combination with temozolomide (TMZ), of glioma (T98G, U118, U138), other cancer (HeLa), and normal (HaCaT) cell lines. We observed the VPA dose-dependent changes in the total DNA methylation in neoplastic cell lines and the lack of such an effect in a normal cell line. VPA at high concentrations (250-500 μM) induced hypermethylation of DNA in a short time frame. However, the exposition of GBM cells to the combination of VPA and TMZ resulted in DNA hypomethylation. At the same time, we observed an increase of genomic 8-oxo-dG, which as a hydroxyl radical reaction product with guanosine residue in DNA suggests a red-ox imbalance in the cancer cells and radical damage of DNA. Our data show that VPA as an HDAC inhibitor does not induce changes only in histone acetylation, but also changes in the state of DNA modification. It shows cross-reactivity between chromatin remodeling due to histone acetylation and DNA methylation. Finally, total DNA cytosine methylation and guanosine oxidation changes in glioma cell lines under VPA treatment suggest a new epigenetic mechanism of that drug action.

Adenovirus-mediated SIRT1 protects cochlear strial marginal cells in a D-gal-induced senescent model in vitro.

A primary obstacle in age-related hearing loss (ARHL) study is the lack of accelerated senescent models in vitro that explore the precise underlying mechanism in different types of ARHL. The damage to strial marginal cells (SMCs) is a subset of strial presbycusis-associated pathological changes. We aimed to establish a D-galactose (D-gal)-induced SMCs senescent model and study the effect of deacetylase sirtuin 1 (SIRT1) on presbycusis in vitro. SMCs from C57BL/6J neonatal mice were cultured and treated with D-gal to establish accelerated senescent models. And then D-gal-induced SMCs were transfected with adenovirus (Ad)-SIRT1-GFP or Ad-GFP. Oxidative stress and mitochondrial DNA (mtDNA) damage were determined by histological analysis or RT-PCR. Western blotting (WB) and RT-PCR were used to evaluate protein and mRNA levels of superoxide dismutase 2 (SOD2) and SIRT1, respectively. Additionally, apoptosis was investigated by WB and TUNEL staining. D-gal-induced SMCs exhibited several characteristics of senescence, including increased the level of 8-hydroxy-2'-deoxyguanosine, which is a marker of DNA oxidative damage, and elevated the amount of mtDNA 3860-bp deletion, which is a common type of mtDNA damage in the auditory system of mice. SIRT1 overexpression effectively inhibited these changes by upregulating the level of SOD2, thereby inhibiting cytochrome c translocation from mitochondria to cytoplasm, inhibiting cell apoptosis, and ultimately delaying aging in the D-gal-induced senescent SMCs. Altogether, the evidence suggests that the D-gal-induced SMCs accelerated aging model is successfully established, and SIRT1 overexpression protects SMCs against oxidative stress by enhancing SOD2 expression in ARHL.

Downhill running induced DNA damage enhances mitochondrial membrane permeability by facilitating ER-mitochondria signaling.

To observe whether downhill running can lead to DNA damage in skeletal muscle cells and changes in mitochondrial membrane permeability and to explore whether the DNA damage caused by downhill running can lead to changes in mitochondrial membrane permeability by regulating the components of the endoplasmic reticulum mitochondrial coupling structure (MAM). A total of 48 male adult Sprague-Dawley rats were randomly divided into a control group (C, n = 8) and a motor group (E, n = 40). Rats in Group E were further divided into 0h (E0), 12h (E12), 24h (E24), 48h (E48) and 72h (E72) after prescribed exercise, with 8 rats in each group. At each time point, flounder muscle was collected under general anaesthesia. The DNA oxidative damage marker 8-hydroxydeoxyguanosine (8-OHdG) was detected by immunofluorescence. The expression levels of the DNA damage-related protein p53 in the nucleus and the EI24 protein and reep1 protein in whole cells were detected by Western blot. The colocalization coefficients of the endoplasmic reticulum protein EI24 and the mitochondrial protein Vdac2 were determined by immunofluorescence double staining, and the concentration of Ca2+ in skeletal muscle mitochondria was detected by a fluorescent probe. Finally, the opening of the mitochondrial membrane permeability transition pore (mPTP) was detected by immunofluorescence. Twelve hours after downhill running, the mitochondrial membrane permeability of the mPTP opened the most (P < 0.05), the content of 8-OHdG in skeletal muscle peaked (P < 0.05), and the levels of the regulatory protein p53, mitochondrial Ca2+, and the EI24 and reep1 proteins peaked (P < 0.01). Moreover, the colocalization coefficients of EI24 and Vdac2 and the Mandes coefficients of the two proteins increased first and then recovered 72h after exercise (P < 0.05). (1) Downhill running can lead to DNA damage in skeletal muscle cells, overload of mitochondrial Ca2+ and large opening of membrane permeability transformation pores. (2) The DNA damage caused by downhill running may result in p53 promoting the transcriptional activation of reep1 and EI24, enhancing the interaction between EI24 and Vdac2, and then leading to an increase in Ca2+ in skeletal muscle mitochondria and the opening of membrane permeability transition pores.

A Biomarker Approach as Responses of Bioindicator Commercial Fish Species to Microplastic Ingestion: Assessing Tissue and Biochemical Relationships

Plastic debris is a growing environmental problem on a global scale, as plastics and microplastics (MPs) can be ingested by marine organisms, inducing toxic effects. The aim of this study was to assess MP intake and antioxidant responses in three bioindicator species: red mullet, bogue, and anchovy (Mullus surmuletus, Boops boops, and Engraulis encrasicolus, respectively) for plastic contamination in the Mediterranean Sea. MP intake was assessed in the gastrointestinal tract of the fish. Further, several enzymes from both the liver and brain were analysed. The antioxidant defences, catalase (CAT) and superoxide dismutase (SOD), as well as the detoxifying enzyme glutathione-S-transferase (GST), were measured in both tissues. The acetylcholine esterase (AchE), as an indicator of neuronal damage, was measured in the brain. Malondialdehyde (MDA) was analysed as a marker of oxidative damage in the brain and liver samples. Total MP intake and MP typology differed between the three species, with M. surmuletus showing the lowest intake of MPs, while B. boops showed the highest intake of MPs. An increase in both antioxidant enzymes was evidenced in E. encrasicolus liver activity with respect to MP intake. In brain samples, an increase in CAT activity was found in M. surmuletus and B. boops as a consequence of MP ingestion. SOD activity in the brain increased in B. boops and E. encrasicolus that had ingested MPs. GST activity increased in the liver of M. surmuletus' and in brains of B. boops that had ingested MPs. The intake of MPs is species related, as well as being inherently linked to the habitat they live in and being able to induce a light activation of species-specific detoxifying and antioxidant mechanisms.

Abstract 10946: Myocardial Inflammatory Activity and Oxidative Stress Immunosuppressive Therapy Are Associated With Prognosis in Patients With Cardiac Sarcoidosis

Background: P atients with cardiac sarcoidosis (CS) have been shown to be at an increased risk of major adverse cardiovascular events (MACE). Enhancement in myocardial inflammatory activity and oxidative stress is a crucial cause of MACE. Immunosuppressive therapy is recommended for the treatment of active CS. After immunosuppressive therapy, however, there is no predictable markers for prognosis. We hypothesized that the inflammation and oxidative stress in heart were associated with MACE. Aim: We identified prognostic markers for MACE in patients with CS after steroid therapy. Methods: This prospective cohort study enrolled 103 consecutive patients with CS diagnosed according to the Japanese guideline; Of 103 CS patients, 39 patients underwent 18F-FDG PET/CT 6 months after steroid therapy, and levels of urinary 8-hydroxy-2′-deoxyguanosine (U-8-OHdG) as a marker of oxidative DNA damage, other biomarkers, indices of cardiac function, and renal function were measured. Then they were followed up for a median of 42 months. The primary endpoint was a composite of the first sustained ventricular tachycardia (sVT) /sudden cardiac death (SCD), hospitalization for heart failure, and worsening CS with increased accumulation of FDG in heart and exacerbation of clinical manifestation. Results: During the follow-up period, 7 of 30 patients showed sVT/SCD (N= 9), hospitalization (N= 2) and worsening CS (N= 4). A Cox proportional-hazard model showed that U-8-OHdG concentration and SUV max value of FDG-PET were independent predictors of MACE. ROC analysis showed that the cut-off values of U-8-OHdG and SUV max for predicting the MACE were 14.2 ng/mg·Cr and 4.6 respectively. Patients with a U-8-OHdG ≥ 14.2 ng/mg·Cr or SUV max ≥4.6 had a significantly higher MACE risk (Figure A and B). Conclusions: U-8-OHdG and SUV max after steroid therapy were powerful predictors of MACE in CS, suggesting that CS patients with high U-8OHdG and/or high SUV max might be resistant to steroid therapy.

LBSUN85 Acipimox Normalizes The Cardiac Phenotype Induced By Electronic Cigarettes

Abstract Electronic nicotine delivery systems or electronic cigarettes (e-cigarettes) are becoming exceptionally popular in the world as an alternative to conventional nicotine cigarettes, both among smokers and people who have never smoked. Nicotine can induce lipolysis in adipose tissue, leading to increased serum free fatty acids (FFAs). Increased levels of FFAs are one of the key elements in generating a pro-inflammatory response and lead to ectopic lipid accumulation, lipotoxicity, mitochondrial dysfunction, and DNA damage. Our laboratory has shown that e-cigarettes induce cardiac dysfunction associated with oxidative stress and inflammatory phenotype. We investigated the effects of acipimox, an antihyperlipidemic drug that blocks lipolysis, on e-cigarettes-induced cardiac dysfunction and its associated inflammatory signals and oxidative stress. C57BL/6J wild type mice on high fat diet were exposed to saline, e-cigarette with nicotine (2.4%), e-cigarette (2.4%) plus acipimox for 12 weeks. Fractional shortening and ejection fraction was decreased in mice exposed to e-cigarette (2.4%) compared with saline and acipimox. Therefore, acipimox normalized the e-cigarette-induced cardiac dysfunction. Transcriptomic evaluation with Gene Set Enrichment Analysis revealed that e-cigarette treated mice had genes enriched in the G2/M DNA damage checkpoint pathways. These transcriptomic changes were normalized by acipimox. Mice exposed to e-cigarettes had increased circulating levels of M-CSF, IL-6, and FFAs, which were decreased by acipimox. Mice exposed to e-cigarette (2.4%) had increased cardiac Heme oxygenase 1, a marker of oxidative stress. Additionally, treatment with e-cigarette (2.4%) increased the apurinic/apyrimidinic sites. This marker of oxidative DNA damage was normalized by acipimox. Understanding the consequences of e-cigarette use on the cardiovascular system is directly relevant to developing policies related to e-cigarette use. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Modulation of biomarkers associated with risk of cancer in humans by olive oil intake: A systematic review

This systematic review summarized the role of olive oil intake in modulation of cancer risk biomarkers in healthy adults. A total of four randomized clinical trials with crossover design were included with intervention periods ranging from three to eight weeks, none of them at high risk of bias. meta-analysis was not performed because the studies were heterogeneous. Results showed that continuous olive oil intake was associated with the reduction of oxidized DNA bases, IL-8, TNF-α, and 8-OH deoxyguanosine, but did not affect ethene-DNA adducts. In summary, this study showed a potential role of olive oil intake by healthy individuals for prevention and repair of cancer-related DNA damage, through lower levels of markers of oxidative DNA damage and inflammation. High levels of these molecules are present and linked with tumor initiation and other carcinogenesis-related events. Therefore, olive oil is a promising agent for cancer risk reduction. To make this association robust, more intervention studies are needed, especially high-quality randomized controlled trials evaluating similar biomarkers over longer periods of time.

Neurotoxic and behavioral deficit in Drosophila melanogaster co-exposed to rotenone and iron.

Exposure to environmental toxicants has been linked with the onset of different neurodegenerative diseases in animals and humans. Here, we evaluated the toxic effects of co-exposure to iron and rotenone at low concentrations in Drosophila melanogaster. Adult wild-type flies were orally exposed to rotenone (50.0 µM) and ferrous sulfate (FeSO4; 1.0 and 10.0 µM) through the diet for 10 days. Thereafter, we evaluated markers of oxidative damage (Hydrogen Peroxide (H2O2), Nitric Oxide (NO), Protein Carbonyl, and malondialdehyde (MDA)), antioxidant status (catalase, Glutathione S-Transferase (GST), Total Thiol (T-SH) and Non-protein Thiol (NPSH), neurotransmission (monoamine oxidase; MAO and acetylcholinesterase, AChE) and mitochondrial respiration. The results indicated that flies fed rotenone and FeSO4 had impaired locomotion, reduced survival rate, and AChE activity with a corresponding increase in MAO activity when compared with the control (p < 0.05). Furthermore, rotenone and FeSO4 significantly decreased the antioxidant status with a concurrent accumulation of NO, MDA, and H2O2. Additionally, the activity of complex 1 and mitochondria bioenergetic capacity was compromised in the flies. These findings suggest that the combination of rotenone and FeSO4 elicited a possible synergistic toxic response in the flies and therefore provided further insights on the use of D. melanogaster in toxicological studies.

Puerarin-V Improve Mitochondrial Respiration and Cardiac Function in a Rat Model of Diabetic Cardiomyopathy via Inhibiting Pyroptosis Pathway through P2X7 Receptors

There is a new form of puerarin, puerarin-V, that has recently been developed, and it is unclear whether puerarin-V has a cardioprotective effect on diabetic cardiomyopathy (DCM). Here, we determined whether puerarin-V had any beneficial influence on the pathophysiology of DCM and explored its possible mechanisms. By injecting 30 mg/kg of STZ intraperitoneally, diabetes was induced in rats. After a week of stability, the rats were injected subcutaneously with ISO (5 mg/kg). We randomly assigned the rats to eight groups: (1) control; (2) model; (3) metformin; (4-6) puerarin-V at different doses; (7) puerarin (API); (8) puerarin injection. DCM rats were found to have severe cardiac insufficiency (arrythmia, decreased LVdP/dt, and increased E/A ratio). In addition, cardiac injury biomarkers (cTn-T, NT-proBNP, AST, LDH, and CK-MB), inflammatory cytokines (IL-1β, IL-18, IL-6, and TNF-α), and oxidative damage markers (MDA, SOD and GSH) were markedly increased. Treatment with puerarin-V positively adjusts these parameters mentioned above by improving cardiac function and mitochondrial respiration, suppressing myocardial inflammation, and maintaining the structural integrity of the cardiac muscle. Moreover, treatment with puerarin-V inhibits the P2X7 receptor-mediated pyroptosis pathway that was upregulated in diabetic hearts. Given these results, the current study lends credence to the idea that puerarin-V can reduce myocardial damage in DCM rats. Furthermore, it was found that the effect of puerarin-V in diabetic cardiomyopathy is better than the API, the puerarin injection, and metformin. Collectively, our research provides a new therapeutic option for the treatment of DCM in clinic.

Lipid accumulation and oxidative stress in the crop tissues of male and female pigeons during incubation and chick-rearing periods

The current study aimed to evaluate the changes in lipid accumulation and oxidative status in pigeon crops during different breeding stages. Forty-two pairs of adult pigeons were randomly assigned to 7 groups. Lipid droplet accumulation in pigeon crops was visualized by using oil red O staining from d 17 of incubation (I17) to d 7 of chick rearing (R7). Transmission electron microscopy analysis showed swollen mitochondria with disintegration of cristae and typical characteristics of endoplasmic reticulum stress in crop tissues at R1 compared with those at I4. During the peak of pigeon milk formation, the concentrations of reactive oxygen species, and oxidative damage markers (advanced oxidation protein products, 8-hydroxy-2 deoxyguanosine, and malondialdehyde) and the enzyme activities of total superoxide dismutase and glutathione peroxidase were all elevated significantly (P < 0.05). The protein concentration of B-cell lymphoma-2 associated X in crop tissues was significantly higher at R1, while the level of B-cell lymphoma-2 protein in males was the highest at I4 (P < 0.05). The ratio of B-cell lymphoma-2 associated X protein (Bax)/B-cell lymphoma-2 (Bcl-2) in both male and female crops peaked at R1 (P < 0.05). Gene expression of the key enzymes involved in mitochondrial and peroxisomal fatty acid β-oxidation was investigated in crops. In males, the gene expression of carnitine palmitoyltransferase 1a peaked at R15, and that of carnitine palmitoyltransferase 2 increased significantly from R1 to R15 (P < 0.05). The mRNA abundance of long chain 3-hydroxyacyl-CoA dehydrogenase increased to the maximum value at R1 and I17 in males and females, respectively. From I17 to R7, the mRNA levels of acyl-CoA oxidase 1 and acyl-CoA oxidase 2 were decreased in pigeon crops (P < 0.05). Conclusively, lipid droplet accumulation was found in male and female pigeon crops from the end of incubation to the early stage of chick rearing. Although antioxidant defence and mitochondrial fatty acid β-oxidation were both mobilized, oxidative stress in crop tissues still occurred during the peak of milk formation.

Pre-Conceptual Guidelines for Men: A Review of Male Infertility Experience, including Nutrition and Lifestyle Factors

Male fertility is declining and affects approximately one in seven couples. Reasons for this are multi-factorial and the subject of on-going research, though environmental contaminants (such xenoestrogens) are believed to be contributory factors. Semen parameters can be improved through a healthy diet and nutritional supplementation has also been shown to improve semen parameters, clinical pregnancy and live birth rates significantly. Despite this, in medical care dietary modification beyond alcohol reduction is rarely recommended. The aim of this review was to consider the psychosocial impacts of infertility in males whilst assessing other nutritional and lifestyle interventions that can be used in personalized nutrition care. More tailored nutrition care needs to consider this and the taboo surrounding the male infertility experience. A systematic approach was used. Three electronic databases (CINAHL, Medline and Academic Search Complete) were searched using predetermined Boolean search terms and identified 125 papers for review. Hand searches were undertaken to ensure recent evidence was included. Duplicates were removed and predefined inclusion and exclusion criteria were applied. Narrative synthesis was used for review and to develop preconceptual guidelines. Review data indicates dietary modification or supplementation with antioxidants such as vitamin C, vitamin E, coenzyme Q10, selenium, carnitine and zinc have been shown to improve markers of male fertility and reduce markers of seminal oxidative damage. Also, a Mediterranean style diet is also associated with higher quality sperm counts. Weight loss is beneficial in terms of normalizing endocrine profiles but at present it is not possible to determine if this is the effect of weight loss alone, or the combined effect of weight loss alongside other dietary improvement. Further research is therefore needed to understand the role of the many potential confounding factors. Despite this, infertility is emotionally challenging for men and nutrition, and personalised nutrition and lifestyle therapies have potential to support men trying to conceive. Pre-conceptual nutrition and lifestyle guidelines for men have been developed from this review and the use should be considered as the basis for more tailored nutrition care in practice.

The Effect of Ramadan Fasting on Serum Malondialdehyde Levels as Indicator of Oxidative Stress and Cellular Damage

Background: Ramadan fasting is one of five pillars of Islam. Fasting is to refrain from eating and drinking from sunrise (sahur) to sunset (ifthar). Ramadan fasting has been shown to impact on body systems in different manners. One of the benefits of Ramadan fasting is protection against oxidative stress and cellular damage. Malondialdehyde (MDA) is a product of free radicals (hydroxil radicals) with polyunsaturated fatty acids (PUFAs) produced from lipid peroxidation of cell membranes. This paper aims to determine the effect of Ramadan fasting on serum MDA levels.Methods: The design of this study is quasiexperimental with one group pre and post design. The sample of this study was 16 preclinical students of FK UIN Syarif Hidayatullah Jakarta who performed Ramadan fasting for 17 consecutive days. Blood samples were taken 1 day before Ramadan fasting and 18 days of Ramadan fasting to measure serum MDA levels. The study was conducted in the biochemical laboratory of FK UIN Syarif Hidayatullah.Results: The mean serum MDA levels before fasting was 0.90 ± 0.54 nmol/mL. The median value of serum MDA levels after fasting was 0.43 nmol/mL, with a range between 0.03 - 2.75 nmol/mL. Ramadan fasting decreases serum MDA levels, but the decrease that occurs on the 17th day of Ramadan fasting was not significant (p&gt; 0.05). There was an increase in serum MDA levels in 4 subjects (25%) after Ramadan fasting.Conclusion: Ramadan fasting can reduce serum MDA levels as a marker of oxidative stress and cell damage. Further study is needed to investigate the various results in serum MDA levels after fasting.

Commelina benghalensis (Wandering Jew) Linn exhibits abortifacient potentials and hepatotoxicity in pregnant Wistar rats via elevating indicators of oxidative stress and activating proinflammatory cytokines

Ethnopharmacological relevanceCommelina benghalensis Linn is a perennial plant with upright stems reaching a height of 1 m. Its stem is commonly used to induce abortion in traditional medicine. However, there are insignificant scientific data to evaluate such a claim. Aim of the studyThe study was conducted to determine the abortifacient and toxicological potential of ethanol extract of Commelina benghalensis Linn stem (EECBS) via selected proinflammatory and oxidative stress biomarkers in pregnant Wistar rats. Materials and methodsTo determine the phytochemicals responsible for EECBS's toxicity and abortifacient effects, high-performance liquid chromatography–photodiode array detection (HPLC-PDA) and gas chromatography-mass spectrometry (GC-MS) was used. The abortion rate was determined by monitoring the markers of reproductive system failure in the experimental model. To assess rat hepatotoxicity, biochemical markers and immunohistopathological parameters were used. ResultsResults demonstrated the presence of isomeric benzene-mesitylene compounds in EECBS. Also, EECBS significantly altered the markers of liver function and oxidative damage while eliciting a significantly reduced (P < 0.05) number of live fetuses, number of corpora lutea, progesterone, estradiol, and luteinizing hormone, whereas the number of dead fetuses percentage vaginal opening, and post-implantation loss increased significantly (P < 0.05). Estrogenicity studies indicated a significant (P < 0.05) increase in uterine weight, uterine glucose, and ALP dose-dependently. Moreover, EECBS also caused a vaginal hemorrhage preceding the parturition. Also, EECBS treatment significantly increased levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and significantly elevated the expression of COX-2 protein in the liver. ConclusionThe current investigation established Commelina benghalensis Linn stem's abortifacient activity. Continuous use, on the other hand, may cause liver damage in pregnant rats by disrupting antioxidant defense mechanisms, promoting the production of pro-inflammatory cytokines, and increasing COX-2 expression. Hence, caution should be excised while consuming this plant's stem for medication purposes, especially during the gestational period.

Creatine supplementation protects against diet-induced non-alcoholic fatty liver but exacerbates alcoholic fatty liver

AimsThis work investigated the effects of creatine supplementation on different pathways related to the pathogenesis of non-alcoholic fatty liver disease and alcoholic liver disease. Main methodsTo induce alcoholic liver disease, male Swiss mice were divided into three groups: control, ethanol and ethanol supplemented with creatine. To induce non-alcoholic fatty liver disease, mice were divided into three groups: control, high-fat diet and high-fat diet supplemented with creatine. Each group consisted of eight animals. In both cases, creatine monohydrate was added to the diets (1 %; weight/vol). Key findingsCreatine supplementation prevented high-fat diet-induced non-alcoholic fatty liver disease progression, demonstrated by attenuated liver fat accumulation and liver damage. On the other hand, when combined with ethanol, creatine supplementation up-regulated key genes related to ethanol metabolism, oxidative stress, inflammation and lipid synthesis, and exacerbated ethanol-induced liver steatosis and damage, demonstrated by increased liver fat accumulation and histopathological score, as well as elevated oxidative damage markers and inflammatory mediators. SignificanceOur results clearly demonstrated creatine supplementation exerts different outcomes in relation to non-alcoholic fatty liver disease and alcoholic liver disease, namely it protects against high-fat diet-induced non-alcoholic fatty liver disease but exacerbates ethanol-induced alcoholic liver disease. The exacerbating effects of the creatine and ethanol combination appear to be related to oxidative stress and inflammation-mediated up-regulation of ethanol metabolism.