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Edited by
Ashok Agarwal, Global Andrology Forum, Ohio, USA,Wael Zohdy, Cairo University, Egypt,Rupin Shah, Well Women’s Clinic, Sir H N Reliance Foundation Hospital, Mumbai
Male infertility is a multifactorial condition, often associated with subtle sperm dysfunction that is not detected by routine semen analysis. Advanced sperm function testing provides deeper insights into key physiological and molecular mechanisms contributing to male reproductive failure. Elevated seminal oxidative stress (OS) is a major contributor to sperm dysfunction and DNA damage. Quantifying OS levels can help individualize treatment intervention. Evaluation of acrosomal enzyme activity offers diagnostic value in cases of unexplained infertility, as these enzymes are essential for oocyte penetration. Sperm chromatin integrity reflects DNA packaging and stability, which are critical for fertilization and early embryogenesis. Lastly, precise regulation of sperm ion channels governs sperm motility and responsiveness to environmental cues; their dysregulation is implicated in male infertility and represents a novel target for contraceptive development. Comprehensive assessment of sperm functions, beyond conventional semen parameters, is valuable in diagnosing and treating male infertility and holds promise for improving diagnostic precision and guiding targeted therapeutic strategies.
Smoking has been confirmed to induce systemic inflammation and oxidative stress (OS) and is associated with higher odds of chronic obstructive pulmonary disease (COPD). Dietary antioxidants can reduce inflammation and OS. This study seeks to score the dietary antioxidant intake and then assess its impact on the association between smoking and COPD in adults. The data extracted from the 2007–2012 National Health and Nutrition Examination Survey database were used. The Dietary Antioxidant Quality Score (DAQS) was evaluated by the total intake of vitamins A, C and E, Se, Zn and Mg in the daily diet. Smoking was used as the exposure variable and COPD as the outcome variable. Weighted multivariable logistic regression was conducted to evaluate the associations of DAQS with smoking and COPD, as well as their joint effects on the odds of COPD. The relationships between dietary antioxidant quality score, smoking status and COPD were subsequently assessed. Subgroup analyses were performed to explore associations between relevant covariates and smoking and COPD across DAQS strata. Current smoking was found to be linked to COPD (OR = 4·06, 95 % CI = 3·14, 5·27) in comparison to never smoking. Among smokers, significant associations were observed in both the medium-quality DAQS group (OR = 3·48, 95 % CI: 2·34, 5·17) and the low-quality DAQS group (OR = 5·60, 95 % CI: 3·58, 8·76). In conclusion, high DAQS levels are inversely related to the odds of COPD in adult smokers. Our findings provide valuable insights for management strategies for COPD.
Oxeiptosis is a reactive oxygen species (ROS)-dependent form of programmed cell death that plays a key role in cellular homeostasis and holds promise as a cancer therapy. This review explores its molecular mechanisms, emphasizing the KEAP1–PGAM5–AIFM1 signalling pathway and its reliance on ROS accumulation. Compared to other cell death pathways, oxeiptosis offers a distinct approach, especially for targeting cancer cells resistant to conventional therapies. The review evaluates emerging inducers, both synthetic and natural, that selectively trigger oxeiptosis in cancer cells. It also examines the potential synergy between oxeiptosis and ROS-generating chemotherapies, particularly in the oxidative tumour microenvironment. However, challenges remain, including identifying tumour-specific inducers, overcoming cancer cell resistance to oxidative stress and reducing off-target effects. The review concludes by highlighting the need for targeted delivery strategies and rigorous preclinical studies to translate oxeiptosis into effective cancer treatments. Overall, it underscores oxeiptosis as a promising avenue to address drug resistance and improve therapeutic outcomes in oncology.
The purpose of this systematic review and meta-analysis was to investigate the effects of hesperidin supplementation on inflammatory and oxidative stress biomarkers in human adults. A systematic literature search was conducted in PubMed, EMBASE and Cochrane Central Register of Controlled Trials from inception to 4 January 2025 to identify eligible randomised controlled trials. Ten randomised controlled trials with a total of 532 participants were included. The results indicated that hesperidin supplementation significantly reduced the serum levels of C-reactive protein or high-sensitivity C-reactive protein (SMD: –0·43; 95 % CI –0·71, –0·15; P = 0·002) and TNF-α (SMD: –0·51; 95 % CI –0·95, –0·07; P = 0·02) in adults, while no significant beneficial effect of hesperidin on IL-6 was observed (SMD: –0·25; 95 % CI –0·52, 0·01; P = 0·06). In addition, hesperidin intake showed a beneficial impact on the IL-6 level in patients with diseases (type 2 diabetes and myocardial infarction) (SMD: –0·38; 95 % CI –0·72, –0·04; P = 0·03) yet not in healthy adults without diagnosed diseases. Our findings demonstrated that hesperidin supplementation could lower the serum levels of C-reactive protein or high-sensitivity C-reactive protein and TNF-α in adults.
Maternal nutrition is critical for foetal brain development, and dietary polyphenolic compounds play an important role in mitigating oxidative stress, inflammation, and neurotoxic damage. This narrative review explored the potential promotion of brain development by polyphenols such as resveratrol, curcumin, quercetin, naringin, ferulic acid, genistein, and fisetin through their antioxidant, anti-inflammatory, and neurotrophic effects. The key molecular mechanisms are central to the advantageous actions of these polyphenols in the neurogenesis process. These compounds protect against neurodevelopmental challenges induced by maternal high-fat diet, immune activation, environmental toxins, and psychological stressors. However, their efficacy may depend on dosage, timing of administration, and maternal-foetal metabolic interactions, emphasising the need for personalised maternal nutrition strategies. Further research is needed to investigate the long-term effects and interactions of these compounds with other nutrients toward personalised maternal nutrition strategies. This narrative review presents the potential of polyphenols to support foetal brain health with an emphasis on their possible incorporation into maternal dietary interventions.
Chrysobalanus icaco L. (Caco) is a fruit tree distributed in tropical areas of Africa and America. Its seeds are a rich source of bioactive compounds, and their consumption could have a positive impact on human health during dyslipidaemias. The objective of this study was to evaluate the hypolipidaemic and antioxidant activities of aqueous extract of Caco seeds in an in vivo model of hypertriglyceridaemia induced by Triton WR-1339 (tyloxapol). Phytochemical characterisation revealed saponin and phytic acid contents of 4730 ± 190 µg of saponin equivalents and 1·0 ± 0·05 µg phytic acid equivalents g–1 of sample, respectively. Phenolic acids and flavonoids (ellagic acid, apigenin-7-O-glucuronide and myricetin, among others) were identified by HPLC-quadrupole time-of-flight (TOF) -MS. Aqueous extract of Caco seeds was administered once daily for three consecutive days at two doses (150 and 600 mg/kg) in male CD1 mice, where treatment with 600 mg/kg reduced serum TAG levels by 64 % compared with control, decreased oxidative damage to lipids and proteins and modulated superoxide dismutase and glutathione peroxidase activity in hepatic tissue. Complementary in silico molecular docking analyses suggested a potential interaction of apigenin-7-O-glucuronide with lipid metabolism-related enzymes. These findings indicate that C. icaco L. seeds may be considered a promising source of bioactive molecules for the treatment and management of early phases of dyslipidaemias, as evidenced in an acute model, but their full potential in chronic stages merits further research.
Major depression (MDD) is linked to neuro-immune, metabolic, and oxidative stress (NIMETOX) pathways. The gut microbiome may contribute to these pathways via leaky gut and immune–metabolic processes.
Aims:
To identify gut microbial alterations in MDD and to quantify functional pathways and enzyme gene families and integrate these with the clinical phenome and immune–metabolic biomarkers of MDD.
Methods:
Shotgun metagenomics with taxonomic profiling was performed in MDD versus controls using MetaPhlAn v4.0.6, and functional profiling was conducted using HUMAnN v3.9, aligning microbial reads to species-specific pangenomes (Bowtie2 v2.5.4) followed by alignment to the UniRef90 v201901 protein database (DIAMOND v2.1.9).
Results:
Gut microbiome diversity, both species richness and evenness, is quite similar between MDD and controls. The top enriched taxa in the multivariate discriminant profile of MDD reflect gut dysbiosis associated with leaky gut and NIMETOX mechanisms, that is, Ruminococcus gnavus, Veillonella rogosaem, and Anaerobutyricum hallii. The top four protective taxa enriched in controls indicate an anti-inflammatory ecosystem and microbiome resilience, that is, Vescimonas coprocola, Coprococcus, Faecalibacterium prausnitzii, and Faecalibacterium parasitized. Pathway analysis indicates loss of barrier protection, antioxidants, and short-chain fatty acids, and activation of NIMETOX pathways. The differential abundance of gene families suggests that there are metabolic distinctions between both groups, indicating aberrations in purine, sugar, and protein metabolism. The gene and pathway scores explain a larger part of the variance in suicidal ideation, recurrence of illness, neurocognitive impairments, immune functions, and atherogenicity.
Conclusion:
The gut microbiome changes might contribute to activated peripheral NIMETOX pathways in MDD.
Cognitive decline is a hallmark of brain ageing. Leucocyte telomere length (LTL) has emerged as a candidate biomarker related to brain ageing and neurodegeneration; however, reported associations with cognition and brain structure vary across cohorts. Long-chain omega-3 polyunsaturated fatty acids (PUFA), notably docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), exert anti-inflammatory and antioxidant effects that may, in some contexts, relate to slower telomere attrition. Here, we synthesise evidence on n-3 PUFA, telomere biology and cognitive outcomes, integrating clinical, epidemiologic and experimental data. We emphasise biological plausibility (oxidative stress/inflammation, membrane remodelling, mitochondrial function and expression of telomerase reverse transcriptase (TERT) through PI3K/Akt/mTOR, NRF2 and epigenetic modifications) while acknowledging heterogeneous human findings and methodological considerations (assay variability, life-course timing, cognitive domains and biomarker stratification). We outline priorities for future studies to clarify causal pathways and inform dietary strategies that support healthy cognitive ageing.
Alterations in the central and peripheral energy metabolism are increasingly recognized as key pathophysiological processes in psychiatric disorders. We investigated mitochondrial respiration and density linked to cellular energy metabolism and oxidative DNA damage in borderline personality disorder (BPD).
Methods
This cross-sectional case–control study compared three groups matched for age and body mass index: women with acute BPD, remitted BPD, and female healthy controls (n = 32, 15, 29). Peripheral blood mononuclear cells were investigated for differences in mitochondrial respiration, density, and markers of oxidative DNA damage.
Results
Participants with acute BPD showed significantly reduced and less efficient mitochondrial ATP production compared to both remitted individuals and controls. Mitochondrial coupling and respiration were inversely associated with oxidative DNA damage, although DNA damage levels did not differ significantly across diagnostic groups. Sensitivity analyses indicated that comorbid major depressive episodes and antidepressant use did not account for the results.
Conclusions
These findings indicate mitochondrial alterations accompany acute symptom severity in BPD and may improve with remission. Unraveling causes and consequences of mitochondrial downregulation and its interplay with DNA maintenance in the context of stress and psychopathology could contribute to novel models and treatment strategies in BPD and related severe psychiatric disorders.
Butachlor is a herbicide extensively employed in rice (Oryza sativa L.) cultivation but historically under-investigated for its toxicological impacts on terrestrial vegetation. This study examines the dose-dependent effects of butachlor on the germination and antioxidant defense mechanisms in the seeds of Asian tape grass [Vallisneria natans (Lour.) H. Hara], an important submerged plant species widely distributed in the agricultural ponds. In a hydroponic setup, seeds were exposed to four concentrations of butachlor (0, 20, 200, and 2,000 μg ai L−1), and cultivated under controlled light conditions to quantify germination rates and assess oxidative stress responses. Our findings showed that butachlor concentrations up to 20 μg L−1 had no effect on the germination rate of V. natans seeds, while germination rates decreased by 6.0% and 8.7% at 200 and 2,000 μg L−1, respectively. At 2,000 μg L−1, malondialdehyde (MDA) content increased by 5.7 nmol g−1 FW, and catalase (CAT) activity declined by 21%, indicating oxidative damage. Additionally, the antioxidants proline (Pro) and glutathione (GSH) were upregulated under 20 μg L−1 butachlor treatment after 12 h, contributing to reactive oxygen species (ROS) scavenging and cellular stability. This study highlights the nuanced interactions between butachlor exposure and the antioxidant defenses in V. natans, providing valuable insights into the ecological impacts of herbicide pollution. Understanding these interactions is crucial for development of sustainable agricultural practices and management of herbicide resistance in aquatic systems.
Catechins are bioactive flavanols commonly found in the fruits and leaves of plants, particularly the fresh tea leaves. This experimental study aims to evaluate the antioxidant properties of epigallocatechin-3-gallate, one of the most prominent catechins, and its ability to mitigate cadmium-induced oxidative stress. Eighty rats were randomly assigned to four groups of 20: an untreated control group (group 1), a catechin-treated group (group 2), a cadmium-exposed group (group 3), and a cadmium-catechin group (group 4). Group 2 rats received daily oral doses of catechin at 300 mg/kg body weight, while Group 3 rats were given an aqueous solution of cadmium chloride at a final concentration of 5 mg/kg body weight (b.w.) per day. Group 4 rats were treated with both catechin and cadmium chloride. The rats in Group 4 exhibited increased levels of total proteins and significant increases in antioxidant markers, including total thiols, glutathione, total antioxidant capacity, superoxide dismutase, glutathione peroxidase, and catalase. Additionally, this group demonstrated significant decreases in blood cadmium levels and in the following enzymes: alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase. They also demonstrated significant decreases in creatinine, blood urea nitrogen, urea, and bilirubin, as well as in oxidation markers (H2O2 and malondialdehyde), compared to the cadmium group (Group 3). Tissue homogenates from the livers and kidneys of Group 4 rats revealed similar results to those of the serum biochemical assay. Based on these findings, it can be concluded that catechin’s (ECGC) antioxidant properties significantly mitigate cadmium-induced oxidative stress.
As the global population ages, the prevalence of cognitive decline is rising, creating urgent demand for proactive strategies that support brain health and healthy ageing. Ergothioneine, a unique dietary amino-thione absorbed via the OCTN1 transporter, has recently gained attention for its potential as a neuroprotective, longevity-promoting compound. This review synthesizes growing evidence from observational, interventional and mechanistic studies. Observational data consistently associate low blood ergothioneine levels with cognitive impairment, neurodegenerative diseases, cardiovascular disorders, frailty and mortality. Interventional trials in older adults suggest that ergothioneine supplementation may improve cognition, memory, sleep quality and stabilize neurodegeneration biomarkers, with no safety concerns at doses up to 25 mg/day. Mechanistic studies reveal that ergothioneine acts through multiple pathways: mitigating oxidative stress, reducing neuroinflammation, preserving mitochondrial function and potentially modulating neurogenesis and NAD+ metabolism, although some mechanisms require further investigation. Beyond cognition, ergothioneine shows promise in supporting other physiological systems relevant to ageing, including cardiovascular, metabolic, gut, eye, auditory, liver, kidney, immune, skin and lung health. Together, current evidence positions ergothioneine as a promising nutritional intervention for promoting cognitive resilience and systemic health in ageing, although larger, long-term interventional trials are needed to confirm causality and optimize use.
Although numerous clinical studies suggest that ginseng supplementation may benefit CVD risk factors, results remain inconclusive. This systematic review and meta-analysis evaluated the effects of ginseng supplementation on CVD-related risk factors. Relevant studies were identified through electronic searches in Embase, Web of Science, Scopus, PubMed and CENTRAL up to August 2024. Statistical analyses, including a random effects model, meta-regression and non-linear modelling, were used to assess heterogeneity, dose–response relationships and the overall effects of ginseng supplementation. A total of 70 studies, published between 1998 and 2024 and involving 4506 participants, were included. Ginseng supplementation significantly affected several biochemical markers, including high-sensitivity C-reactive protein (standardised mean difference (SMD): −0·23; 95 % CI: −0·38, −0·08; P = 0·002), gamma-glutamyl transferase (SMD: −0·20; 95 % CI: −0·36, −0·04; P = 0·015), glutathione reductase (SMD: 0·90; 95 % CI: 0·38, 1·42; P = 0·001), reactive oxygen species (SMD: −0·94; 95 % CI: −1·27, −0·60; P < 0·001) and superoxide dismutase (SMD: 0·48; 95 % CI: 0·10, 0·87; P = 0·014). Meta-regression analysis showed significant linear associations between ginseng dosage and Homeostatic Model Assessment for Insulin Resistance (P = 0·044) and between supplementation duration and malondialdehyde (P = 0·007). Dose–response analysis revealed significant associations between ginseng dose and fasting blood glucose (P < 0·001), high-sensitivity C-reactive protein (P = 0·043), IL-6 (P = 0·041), diastolic blood pressure (P = 0·022), IL-10 (P = 0·048), fasting insulin (P = 0·012) and total protein (P = 0·010). Supplementation duration was positively associated with malondialdehyde levels (P = 0·008). Ginseng supplementation was associated with improvements in inflammatory markers, liver function and oxidative stress parameters. No significant effects were observed on anthropometric indices, blood pressure, glycaemic profile, lipid profile, adipokines or heart rate.
There are differences in IgA responses to tryptophan catabolites (TRYCATs) in major neurocognitive psychosis (MNP) versus simple neurocognitive psychosis (SNP) and normal controls. MNP and SNP are distinct schizophrenia classes which are differentiated by neurocognitive deficits, phenome features, and biomarker pathways. Nevertheless, there is no data on serum concentrations of those TRYCATs in MNP and SNP. The aim of the present study is to examine serum concentrations of tryptophan and TRYCATs in MNP versus SNP and controls.
Methods:
This case-control study examines serum levels of tryptophan and TRYCATs in 52 MNP patients, 68 SNP patients and 60 controls in association with overall severity of schizophrenia (OSOS).
Results:
MNP patients show lower tryptophan, kynurenic acid (KA), 3-OH-anthranilic acid (3HAA), and higher anthranilic acid (AA) and quinolinic acid (QA) than SNP patients and controls. There were no differences between SNP and controls in these TRYCATs. Kynurenine (KYN) was lower in MNP+SNP than in controls. We found that 36.5% of the variance in OSOS was explained by the combined effects of lowered tryptophan, KA, and 3-HK, and increased QA and AA. The most important biomarkers of MNP and OSOS were the QA/KA ratio followed by the QA/3HAA ratio.
Conclusions:
The alterations in serum TRYCAT levels further emphasize that MNP and SNP represent two biologically distinct subtypes of schizophrenia. The reductions in TRYCATs diminish the antioxidant and immunoregulatory functions of the TRYCAT pathway. Elevated QA levels may exacerbate the disruption of the blood-brain barrier and the immune-related and oxidative neurotoxicity in MNP.
Excessive zinc (Zn) intake can lead to Zn toxicity, causing adverse effects in gastrointestinal system. To date, there remains no definitive consensus on the mechanisms by which Zn overload induces cell death and intestinal injury. This study was to assess the toxicity mechanism of Zn overload in intestine, with a particular concentrate on oxidative stress and energy metabolism. We first explore the effects of short- and long-term Zn imbalances on intestinal health in mice. We found that the Zn imbalances resulted in oxidative damage, and impaired ketoglutarate dehydrogenase (α-KGDH) activity, which collectively contributed to a detrimental impact on the integrity of the intestinal barrier in mice. We next determined the dynamics of oxidative stress and energy metabolism in Zn overload treatment IPEC-J2 cells. Excessive Zn activated reactive oxygen species (ROS) overproduction and the PKC-NOX oxidative stress pathway. Moreover, the increase of mitochondrial Zn2+ caused mitochondrial ROS accumulation and influenced the expressions of α-KGDH andisocitrate dehydrogenase (IDH), two pivotal rate-limiting enzymes in tricarboxylic acid (TCA) cycle. Zn overload also significantly inhibited the expressions of key nicotinamide adenine dinucleotide (NAD+) synthesis enzymes, namely NMNAT1 and NAMPT, leading to a notable decline of NAD+ and ATP. Furthermore, rescue experiments showed supplementation of NAD+ or boosting NAD+ synthesis, but not antioxidants addition, could rescue Zn toxicity. The collective findings suggest NAD+ reduction is the primary factor contributing to intestinal Zn toxicity, although ROS also plays a role. This indicates that the modulation of NAD+ synthesis may prove an effective strategy for the minimization or elimination of Zn toxicity.
The objective was to evaluate the use of resveratrol conjugated with silica nanoparticles during the in vitro maturation of bovine oocytes. The oocytes were divided into the following treatment groups during the maturation process: control (n = 159), resveratrol 0.5 μM (n = 158), resveratrol 1 μM (n = 155), nanoparticles conjugated with 0.5 μM resveratrol (n = 159), and nanoparticles conjugated with 1 μM resveratrol (n = 158). Several parameters were assessed, including cumulus oophorus size, reactive oxygen species (ROS) production, oocyte nuclear maturation, cell apoptosis, cleavage rates, and blastocyst production rates. Statistical analysis was conducted using Sigma Plot software (version 11) and SAS Studio, with statistical significance defined as P ≤ 0.05 for the main effects and interactions. The results indicated that the cumulus oophorus size was smaller in the resveratrol 1 μM treatment group, and the oocyte size was reduced in the nanoparticle 1 μM treatment group. No significant differences were detected between the treatment groups in terms of ROS production, oocyte maturation, or cell apoptosis. However, the resveratrol 1 μM treatment group exhibited decreased rates of cleavage and blastocyst formation. In contrast, the nanoparticles 0.5 μM and 1.0 μM treatments showed improved cleavage and blastocyst rates compared with the resveratrol 1.0 μM treatment group. In summary, while resveratrol alone at 1 μM concentration had a negative impact on cleavage and blastocyst rates, the use of silica nanoparticles conjugated with resveratrol (both 0.5 μM and 1 μM) enhanced these outcomes, suggesting a potential advantage in using nanoparticle-conjugated resveratrol for the in vitro maturation of bovine oocytes.
The extracellular matrices, such as the haemolymph, in insects are at the centre of most physiological processes and are protected from oxidative stress by the extracellular antioxidant enzymes. In this study, we identified two secreted superoxide dismutase genes (PxSOD3 and PxSOD5) and investigated the oxidative stress induced by chlorpyrifos (CPF) in the aquatic insect Protohermes xanthodes (Megaloptera: Corydalidae). PxSOD3 and PxSOD5 contain the signal peptides at the N-terminus. Structure analysis revealed that PxSOD3 and PxSOD5 contain the conserved CuZn-SOD domain, which is mainly composed of β-sheets and has conserved copper and zinc binding sites. Both PxSOD3 and PxSOD5 are predicted to be soluble proteins located in the extracellular space. After exposure to different concentrations of sublethal CPF, MDA content in P. xanthodes larvae were increased in a dose-dependent manner; SOD and CAT activities were also higher in CPF-treated groups than that in the no CPF control, indicating that sublethal CPF induces oxidative stress in P. xanthodes larvae. Furthermore, PxSOD3 and PxSOD5 expression levels and haemolymph SOD activity in the larvae were downregulated by sublethal CPF at different concentrations. Our results suggest that the PxSOD3 and PxSOD5 are putative extracellular antioxidant enzymes that may play a role in maintaining the oxidative balance in the extracellular space. Sublethal CPF may induce oxidative stress in the extracellular space of P. xanthodes by reducing the gene expression and catalytic activity of extracellular SODs.
The development of oxidative stress depends on the deregulation of the fine balance between the proportion of reactive oxygen species (ROS) generation and the activity of antioxidants. As oxidative stress is deleterious for Leishmania sp., their host cell generates ROS as one of the foremost defence strategies. The parasites have also raised a variety of counteracting tricks in order to conquer this challenge. Upon infection, the host’s own antioxidant system is activated by the parasite to neutralise the oxidative stress-mediated protection. In addition to using the host’s antioxidant mechanisms, some genes within the parasite also make them more tolerant against oxidative stress. Therefore, the present review focuses on some major regulators intimately related to the equilibrium between oxidation and antioxidation following infection with Leishmania sp., which may be helpful in developing a comprehensive knowledge of this specific wing of infection biology associated with oxidative stress.
Search Results
Reactive oxygen species (ROS) play a dual role in leishmaniasis by contributing to both host defence and parasite survival mechanisms. In the host, ROS promote parasite clearance through induction of apoptosis, activation of pro-inflammatory signalling pathways (e.g., MAPK, JNK), inflammasome assembly, and M1 macrophage polarisation. Conversely, Leishmania species have evolved multiple strategies to neutralize ROS, including the upregulation of host antioxidant enzymes like HO-1, inhibition of ROS-producing pathways, and expression of parasite-derived antioxidants such as SOD, GPx, and trypanothione reductase. The parasite alsoadapts through gene regulation and metabolic changes to counter oxidative stress. Importantly, ROS have emerged as key targets for antileishmanial therapies, with various drugs and natural compounds shown to induce ROS-mediated parasite death, highlighting their potential in future therapeutic development.
Conclusions
In summary, the survival of Leishmania hinges on its ability to counteract host-induced oxidative stress. Targeting its antioxidant defences and enhancing host ROS production can disrupt this balance, leading to parasite death. Exploring ROS-related signalling offers a promising path for developing effective therapies against leishmaniasis.
This study aimed to evaluate the effects of acetyl-L-carnitine on follicle survival and growth, stromal cell density and extracellular matrix, as well as on the expression of mRNA for nuclear factor erythroid 2-related factor (NRF2), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and peroxiredoxin 6 (PRDX6) in cultured bovine ovarian cortical tissues. Ovarian fragments (3 × 3 × 1 mm) were cultured for 6 days in α-MEM+ alone or supplemented with 10, 50 or 100 μM acetyl-L-carnitine at 38.5°C with 5% CO2 in humidified air. Before (non-cultured tissues) and after culture, the ovarian fragments were fixed in 4% paraformaldehyde for 12 h for histological analysis or stored at –80ºC for mRNA expression analysis of NRF2, SOD, CAT, PRDX6 and GPX1. The results showed that 100 μM acetyl-L-carnitine increased the percentages of morphologically normal follicles and stromal cell density in cultured ovarian tissues. On the other hand, acetyl-L-carnitine did not influence the percentage of collagen in ovarian tissue nor the expression of mRNAs for NRF2, SOD, CAT, PRDX6 and GPX1. In conclusion, 100 μM acetyl-L-carnitine increased follicle survival and stromal cell density in cultured bovine ovarian tissues but does not influence collagen fibre distribution or the expression of mRNAs for NRF2, SOD, CAT, PRDX6 and GPX1.