Changes In Oxidative Stress Parameters Research Articles

EGCG alleviates Ochratoxin A-induced pyroptosis in rat's kidney by inhibiting NLRP3/Caspase-1/GSDMD signaling pathway

Ochratoxin A (OTA) exposure is inevitable due to its contamination in foods, and there is no treatment for the OTA induced organ toxicity. We evaluate the effect of epigallocatechin gallate (EGCG) on the nephrotoxicity caused by OTA, and to reveal the relationship of this effect with the NLRP3/Caspase-1/GSDMD pathway dependent pyroptosis. 40 male Wistar albino rats divided into 5 groups (n = 8, per group) 0.5 mg/kg/day OTA were administered to the rats and 50 mg/kg and 100 mg/kg EGCG were administered to the groups by gavage orally for 14 days. Serum urea and creatinine levels increased significantly with OTA exposure. Similarly, it was determined that significant changes in oxidative stress parameters with OTA exposure in kidney tissue. Also, there was a significant increase in kidney tissue TGF-β, NF-κB, IL-1β, IL-18, NLRP3, Caspase-1 and GSDMD mRNA expressions with OTA exposure. EGCG administration augmented a dose-dependent decrease in the aforementioned parameters. NLRP3/Caspase-1/GSDMD pathway is induced in the kidneys due to OTA exposure were shown with this study. Potent antioxidant EGCG could alleviate the pathways specified with this study in OTA nephrotoxicity and its supplementation may be effective strategies for the protection.

Secukinumab Ameliorates Oxidative Damage Induced by Subarachnoid Hemorrhage

This study aimed to investigate the histological and biochemical neuroprotective effects of secukinumab (SEC) on brain damage induced by subarachnoid hemorrhage (SAH) in male Wistar Albino rats. Forty male Wistar Albino rats were randomly divided into 4 groups of equal size: control, SEC, SAH, and SAH+SEC. SAH was induced the SAH and SAH+SEC groups by injecting autologous blood collected from the hearts of the rats into the subarachnoid space via the foramen magnum. SEC was administered intraperitoneally once a week to the SEC and SAH+SEC groups after the surgical procedure. On the 14th day of surgery, the rats were sacrificed and their cerebral tissues were collected for biochemical analysis and histopathological examination. SAH led to changes in oxidative stress parameters by increasing malondialdehyde levels and decreasing superoxide dismutase, glutathione, catalase, and glutathione peroxidase levels. Histopathologically, cerebral tissues in the SAH groups showed alterations such as congestion and cell infiltration. Treatment with SEC significantly reduced malondialdehyde levels and increased superoxide dismutase, glutathione, catalase, and glutathione peroxidase levels. SEC also decreased histopathological alterations in brain tissues. This study revealed that SEC (3mg/kg) therapeutically influenced oxidative and histopathological changes in blood parameters and brain tissues caused by experimental SAH. SEC helps reduce brain damage in rats with SAH and possesses antioxidant and neuroprotective properties. Further advanced studies are needed to prove its potential benefits for humans.

Influence of Selected Natural Antioxidants on Iron-Induced Enzymatic Alterations Related to Oxidative Stress

Iron is required in various biological processes of the cell, but excess iron causes oxidative stress. Oxidative stress can be prevented by antioxidants with free radical scavenging properties. Tannic acid and gallic acid are phenolic compounds with antioxidant properties found naturally in plants. In this study, the effects of gallic acid and tannic acid on iron-induced oxidative stress parameters were investigated in a fruit fly model. Effect of the compounds against iron-induced oxidative stress were evaluated by determining spectrophotometrically superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetylcholinesterase (AChE) enzyme activities, and levels of reduced glutathione (GSH) and malondialdehyde (MDA) in larvae (n: 10) and adults (n: 20) of wild type Oregon R strain of Drosophila melanogaster. Iron treatment decreased enzyme activities and GSH levels, but increased MDA levels. Co-treatment of these compounds with iron ameliorated iron-induced changes, especially in larvae. On the other hand, iron-induced decrease in AChE activity was increased in adults by treatment of these compounds with iron. The results showed that natural phenolic compounds have the potential to ameliorate iron-induced changes in oxidative stress parameters.

Sleep Deprivation-Induced Oxidative Stress in Rat Models: A Scoping Systematic Review.

Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist (inactivity, energy conservation, restoration, brain plasticity and antioxidant), multiple unknowns still remain regarding the proposed antioxidant roles of sleep. The existing experimental evidence is often contradicting, with studies pointing both toward and against the presence of oxidative stress after sleep deprivation. The main goals of this review were to analyze the existing experimental data regarding the relationship between sleep deprivation and oxidative stress, to attempt to further clarify multiple aspects surrounding this relationship and to identify current knowledge gaps. Systematic searches were conducted in three major online databases for experimental studies performed on rat models with oxidative stress measurements, published between 2015 and 2022. A total of 54 studies were included in the review. Most results seem to point to changes in oxidative stress parameters after sleep deprivation, further suggesting an antioxidant role of sleep. Alterations in these parameters were observed in both paradoxical and total sleep deprivation protocols and in multiple rat strains. Furthermore, the effects of sleep deprivation seem to extend beyond the central nervous system, affecting multiple other body sites in the periphery. Sleep recovery seems to be characterized by an increased variability, with the presence of both normalizations in some parameters and long-lasting changes after sleep deprivation. Surprisingly, most studies revealed the presence of a stress response following sleep deprivation. However, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear. While a definitive exclusion of the influence of the sleep deprivation protocol on the stress response is not possible, the available data seem to suggest that the observed stress response may be determined by sleep deprivation itself as opposed to the experimental conditions. Due to this fact, the observed oxidative changes could be attributed directly to sleep deprivation.

Changes in Oxidative Stress Parameters in Terms of Simultaneous Exposure to Physical and Chemical Factors: A Systematic Review.

Physical and chemical factors of workplace, either alone or in combination, contribute to oxidative stress that is harmful to the body. The combined impact of physical and chemical components of the work environment on oxidative stress was examined in this research. Research articles published from 2000 to 2021 on this topic in reliable national and international databases were collected and analyzed. Based on the preliminary screening, 120 articles were selected for the first stage. The relevance and quality of 85 suitable papers were found appropriate and evaluated by examining the purpose of the study in the next phase. The data collected and presented from the articles cover simultaneous exposure to physical risk factors such as noise, radiation, and chemicals such as metal solvents, as well as different types of oxidative stress parameters like MDA, GHS, LOP, 8-OHdG, SOD, CAT, ROS, and other parameters such as research site, co-exposure effects, and target organ. Investigating the combined effect of physical and chemical variables on oxidative stress in the target organs, as well as the interaction of multiple effects on each other, was one of the key goals of the articles (synergistic, reinforcing, additive or antagonistic). Most of the findings of theses researches generally highlight the synergistic impact of concurrent exposure to chemical and physical risk factors on oxidative stress.

Determinants Related to Oxidative Stress Parameters in Pediatric Patients with Type 1 Diabetes Mellitus

Adequate glycemic management is one of the main goals in treating type 1 diabetes mellitus (T1DM) and preventing the early onset of diabetic complications. Improperly controlled diabetes mellitus (DM) will result in oxidative stress (OS) and lead to further related health issues. Therefore, the aim of this study was to evaluate the body’s ability to defend against OS depending on the duration of T1DM, metabolic management, antioxidant intake and modern glycemic monitoring systems (GMS). The study included 103 adolescents with T1DM aged 10–17 years. The control group consisted of 65 healthy peers. The patients’ blood was assayed for antioxidant enzymes, minerals and toxic elements. In addition, their dietary intake of antioxidant components was assessed. The T1DM group had higher total oxidant status, oxidative stress index and Cu/Zn ratio values, higher concentrations of malondialdehyde and lower total antioxidant status (TAS) and chromium, zinc, superoxide dismutase and catalase levels than their healthy peers. The comparison between GMS types revealed favorable changes in OS parameters for the flash and continuous systems. Furthermore, an effect of vitamin A and C dietary intake on serum TAS concentrations was detected. More than 82% of the patients with high TAS fulfilled the estimated average requirement norm for vitamin A, and more than 60% fulfilled the vitamin C requirement. In youths with T1DM, it is advisable to observe the antioxidant activity of the body to prevent the accelerated development of diabetic complications.

Effects of Flavobacterium psychrophilum extracellular products and lipopolysaccharide antigens on the antioxidant enzyme system activity of rainbow trout (Oncorhynchus mykiss) fry

The aim of this study was to investigate the response of different doses of lipopolysaccharide (LPS) and extracellular product (ECP) antigens (25, 50, 100, 250, and 500 µg) obtained from Flavobacterium psychrophilum to changes in oxidative stress parameters (catalase [CAT], superoxide dismutase [SOD], glutathione peroxidase [GPx], glucose 6-phosphate dehydrogenase [G6PD], glutathione reductase [GR], and malondialdehyde [MDA]) in juvenile rainbow trout. For this purpose, 6 different doses of F. psychrophilum (102–106) were applied to the fish, and the lethal dose 50 % (LD50) value was determined as 1.33·104. Changes in MDA levels and antioxidant enzymes were determined by applying 25 % of the LD50 value to fish for 14 days. Accordingly, while F. psychrophilum increased GR, G6PD, GPx, and SOD activity, it decreased MDA levels and CAT activity. Initially, 25, 50, 100, 250, and 500 µg doses of ECP and LPS were applied to the fish; after 21 days, a 25 % dose of LD50 was applied to these fish. Fourteen days later, the fish were taken, and the changes in MDA levels and antioxidant enzymes were examined. As a result, it was determined that while ECP and LPS application decreased GR, G6PD, GPx, and SOD activity, there was an increase in MDA levels and CAT activity.

Early time course of oxidative stress in hippocampal synaptosomes and cognitive loss following impaired insulin signaling in rats: Development of sporadic Alzheimer’s disease

Oxidative stress, caused by impaired insulin signaling, plays a pivotal role in the pathogenesis of sporadic Alzheimer’s disease (sAD). We investigated the oxidative stress parameters in the synaptosomes prepared from the hippocampus tissue in order to identify their potential role in sAD development in intraperitoneal (IP) and intracerebroventricular (ICV) streptozotocin (STZ) injections models of insulin signaling impairment. Rats were harvested 1, 3, or 6 weeks post treatment. Spatial learning and memory, several antioxidants and oxidative stress markers were analyzed. Results showed a significant deficit in learning and memory in rats injected with STZ through IP and ICV routes. Glutathione, glutathione/oxidized glutathione, glutathione S-transferase, glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase(SOD)-total, Zn/Cu(SOD), Mn/Fe(SOD) are significantly decreased in IP-STZ and ICV-STZ groups at 1, 3, and 6 weeks after STZ injection. Oxidized glutathione, thiobarbituric acid reactive species, glucose 6-Phosphate dehydrogenase, protein carbonyls, 4-Hydroxynonenal, and 3-Nitrotyrosine are significantly increased in IP-STZ and ICV-STZ groups at 1,3, and 6 weeks after STZ injection. Changes in oxidative stress parameters in ICV-STZ groups are greater than IP-STZ groups. STZ treatment induced cognitive impairments by 3-W and 6-W, and it was significantly correlated with the extent of oxidative damage. In conclusion, STZ administration through ICV route is deleterious in causing early synaptosomal oxidative damage that exacerbated with time and correlated with cognitive impairments. Our data implicate the involvement of oxidative stress as an early feature of sAD and provide insights into the behavioral and biochemical changes over the course of disease development.

Impact of polystyrene microplastic exposure on lipid profile and oxidative stress status of male and female Wistar rats.

Microplastics (MPs) are currently global environmental pollutants, and their associated health risks cannot be ignored. However, research on MP toxicity in mammals is limited. We investigated the effects of polystyrene microplastic (PS-MP) particles on the lipid profile and oxidative stress markers of Wistar rats. Two forms of PS-MP-pristine polystyrene and Styrofoam microplastics-particles of diameter <5 mm were used in this study. Each form was separately incorporated into rat feed in varying proportions of 1, 5 and 10%. A total of seventy rats (thirty-five male and thirty-five female rats) were used for this study and were separately distributed into seven groups of five rats each. The rats were then randomly assigned to a control group which received normal rat feed and water and six (6) test groups which were fed varying percentages (1, 5 and 10) of polystyrene microplastics diet for a period of 90 days. The rats were sacrificed under mild diethyl ether anesthesia 12 hr after cessation of treatment and blood was collected for lipid profile and oxidative stress analyses. Results obtained showed that oral exposure to microplastics caused decreased high density lipoprotein cholesterol (HDL-C) and increased low density lipoprotein cholesterol (LDL-C) in the rats. In contrast, there were no significant changes in oxidative stress parameters in the rats following microplastics exposure. Atherogenic indices in the PS-MP exposed rats differed according to gender. These results indicated that PS-MP dietary exposure may lead to dyslipidemia and male rats had higher cardiovascular risk.

The effects of chronic nanoselenium treatment on sciatic nerve injury: behavioral and biochemical responses

BackgroundNanoselenium as a free radical scavenger suggested being a neuroprotective agent in some neuronal diseases. As the neuropathic pain could be a consequence of a defect in antioxidant defenses and changes in oxidative stress parameters, the present study was planned to investigate the effect of nanoselenium particles on pain-related behaviors and spinal antioxidant defense parameters in the sciatic nerve injury model.MethodsAdult male albino Wistar rats (n = 32) were randomly allocated to the four experimental groups: control group, neuropathy group with chronic constriction injury of the sciatic nerve (CCI), CCI + nanoselenium, CCI + vehicle. The CCI model was used to create neuropathic pain-related symptoms. Nanoselenium or vehicle was injected intraperitoneally for 14 days. The behavioral evaluation was carried out to assess the pain threshold by the radiant heat and von Frey tests. Malondialdehyde (MAD), superoxide dismutase (SOD) levels, and catalase activity in the spinal cord were evaluated to investigate the possible relation.ResultsOur data displayed that CCI triggered neuropathic pain-related behaviors in rats. Chronic treatment with nanoselenium meaningfully improved pain threshold (P < 0.001; F = 37.86, F = 29. 82) and decreased the level of MDA (P < 0.01; F = 33.16) and increased the SOD level (P < 0.001; F = 13.43) and catalase activity (P < 0. 05; F = 10.17) in the spinal cord of CCI rats.ConclusionChronic nanoselenium treatment can improve pain-related behavior and is associated with a reduction in MDA level and increasing in SOD level and catalase activity in the spinal cord of the CCI rats. Nanoselenium provides a therapeutic alternative for the treatment of neuropathic pain by alteration in lipid peroxidation and antioxidant defense system factors.

Oxidative stress in neonatal lambs and its relation to health status and passive colostral immunity

Oxidative stress (OS) related to birth in ruminants may increase susceptibility to diseases. However, information about the physiological changes related to OS in lambs is limited. This study was designed to evaluate changes in OS parameters [total antioxidant status (TAS, mmol Trolox Equiv./L), total oxidant status (TOS, μmol H2O2 Equiv./L)] and calculated oxidative stress index (OSi = TOS/TAS * 100, Arbitrary Unit) and its association with passive colostral transfer immunity and health status in neonatal Akkaraman crossbreed lambs. Control group of healthy lambs (n = 15) were blood sampled before (day 0) and after colostrum intake (on day 1, 2, 4, 7, 14 and 28) in order to evaluate the effect of colostrum intake on TAS, TOS and OSi over time. In addition, a group of lambs (experimental group, n = 60), based on their health status and different cut off value of IgG (mg/dL), was also blood sampled at 24 ± 1 h of colostrum ingestion to determine the relationship between OS parameters, IgG and health status.OS was evident at birth and gradually decreased in control group as TOS (days 0:8.06 ± 0.64, 1:7.05 ± 0.51, 2:5.23 ± 0.35, 4:5.05 ± 0.2, 7:5.13 ± 0.34, 14:3.75 ± 0.12 and 28:3.73 ± 0.15 μmol H2O2 Equiv./L), OSi (days 0: 8.35 ± 0.64, 1: 9.17 ± 1.05, 2:6.83 ± 0.6, 4:6.30 ± 0.20, 7:6.67 ± 0.59, 14:4.46 ± 0.19 and 28:4.87 ± 0.29 au) and TAS (days 0: 0.97 ± 0.02, 1:0.82 ± 0.04, 2:0.81 ± 0.05, 4:0.81 ± 0.02, 7:0.80 ± 0.03, 14:0.85 ± 0.02 and 28:0.79 ± 0.03 mmol Trolox Equiv./L) values changed over time. In the experimental group, the lambs died in the first week of the neonatal period had higher levels of TOS (10.3 ± 0.90 μmol H2O2 Equiv./L) and OSi (1.61 ± 0.22 au) than healthy ones (TOS:6.90 ± 0.36 μmol H2O2 Equiv./L, OSi:1.12 ± 0.11 au) (P < 0.001). The gradual decrease in OS in the neonatal period was accepted as a sign of improved antioxidant response. The study disclosed that deaths may develop when OS at birth is not balanced by suffıcient amount and quality of colostrum an important source of antioxidants such as enzymes and vitamins. The study presented may provide new information in the field of study on oxidative stress in neonatal lambs and help to prevent deaths in the first week of life. It can also be useful in developing preventive measures such as supplements of antioxidants to colostrum.

Role of ultraviolet ray filters and antioxidants in the prevention of DNA damage and oxidative stress associated with phototherapy in jaundiced term neonates

Background Phototherapy induces DNA damage by direct and indirect (oxidative) effects, which are prevented by ultraviolet (UV) filters and antioxidants. Aim Our goal was to assess DNA damage and oxidative stress associated with phototherapy and to prove the efficacy of UV filters and antioxidants for the prevention of DNA damage. Patients and methods The study included 160 jaundiced neonates who had been exposed to phototherapy for at least 48 h. The neonates were divided into four groups, 40 neonates in each group. The first (control) group received phototherapy only; the second group received antioxidants before and during phototherapy; the third group received phototherapy under an umbrella of UV filters; and the fourth group received phototherapy under both UV filters and antioxidants. DNA damage was assayed by the comet assay. Plasma total antioxidant capacity and total oxidant status levels were also measured and then oxidative stress index was calculated for all the four groups before and 48 h after phototherapy. Results The first group showed significant DNA damage accompanied with severe deterioration in all oxidative stress parameters by about 19%; the second group showed a decreasing trend as regards DNA damage and oxidative stress parameter deterioration to about 9%; the third group showed a more decreasing trend than group II to about 5%; but on the other hand, the fourth group showed complete DNA protection from damage with no changes in oxidative stress parameters. Conclusion Phototherapy causes DNA damage that can be completely prevented by combined concurrent use of UV filters and antioxidants.

The effects of imidacloprid on 8-hydroxy-2-eoxyguanosine (8-OHdG) and antioxidant parameters in gill and liver tissues of trout

ABSTRACT In this research, it was aimed to determine the effects of imidacloprid on 8-hydroxy-2-deoxyguanosine (8-ohdg) and antioxidant parameters in the liver and gill tissues of rainbow trout (Oncorhynchus mykiss). Three different concentrations (5 mg/L, 10 mg/ L and 20 mg/L) of the imidacloprid were routinely exposed to rainbow trout for 21 days. Antioxidant enzymes, malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHDG) were studied in the samples. In the 5 mg/L experimental group, it was determined that CAT values and liver GPx and SOD levels increased compared to those in the control group. It was found that there were significant increases between 5 mg/L and 10 mg/L dose groups of MDA, 8-OHdG, liver GPx-SOD and gill CAT-GPx enzyme activities (p < 0.05). High increases in all antioxidant enzyme levels were observed in liver and gill tissues of fish exposed to 20 mg/L dose imidacloprid. 8-OHdG and MDA levels significantly increased in parallel with the increase in the dose (p <0.05). These results suggested that imidacloprid can be toxic to fish by leading to an increase in 8-OHdG activity and changes in oxidative stress parameters. Therefore, these data may reflect one of the molecular pathway that play roles in imidacloprid toxicity.

Sex-specific changes in oxidative stress parameters and longevity produced by Bisphenol F and S compared to Bisphenol A in Drosophila melanogaster

Female and male Drosophila melanogaster were exposed separately for seven days to Bisphenol A (BPA), Bisphenol F (BPF), and Bisphenol S (BPS) at concentrations of 0.25, 0.5, and 1 mM. We observed that males exposed to 0.5 and 1 mM BPS showed lower catalase (CAT) activity and higher superoxide dismutase (SOD) and reactive species (RS); CAT activity decreased for BPF 0.5 and 1 mM. Nevertheless, BPA 0.5 and 1 mM decreased CAT activity, increased RS and lipid peroxidation (LPO), and reduced mitochondrial viability. None of the bisphenols altered the cell viability of male flies, although BPA 0.5 and 1 mM reduced longevity. In female flies, BPA and BPS 0.5 and 1 mM increased RS and LPO levels and decreased CAT activity and glutathione-S-transferase (GST), which may have contributed to lower mitochondrial and cell viability. Furthermore, BPS decreased SOD activity at the 1 mM concentration, and BPA reduced the SOD activity at concentrations of 0.5 and 1 mM. In the BPF 1 mM group, there was a reduction in GST activity and an increase in RS and LPO levels. The toxicological effects were different between sexes, and BPA was more harmful than BPF and BPS in male flies. Thus, our findings showed that females were more susceptible to oxidative cell damage when exposed to BPA and BPS than to BPF, and daily exposure to BPA and BPS at all concentrations reduced female longevity, as well as in BPF 1 mM.

Jobelyn® extends the life span and improves motor function in Drosophila melanogaster exposed to lipopolysaccharide via augmentation of antioxidant status.

Jobelyn® (JB), a dietary supplement, derived from polyphenol-rich leaf sheath of Sorghum bicolor, has been reported to attenuate sensorimotor deficits and oxidative stress evoked by complete Freund-adjuvant in mice. This present study evaluated its effects on the life span, motor function and changes in oxidative stress parameters as well as acetylcholinesterase activity in Drosophila melanogaster exposed to lipopolysaccharide (LPS). The flies (50 per vial), in 5 replicates were fed with LPS (250μg/kg diet) alone or in combination with JB (0.25-1.0mg/kg diet) daily for 7days. The mortality rate and motor function were evaluated on day 7. The flies were afterwards processed for determination of oxidative stress parameters and acetylcholinesterase activity. The effects of JB (0.25-1.0mg/g diet) on the longevity of Drosophila was also investigated wherein the flies were monitored daily for mortality throughout their lifespan. The flies exposed to LPS (250μg/kg diet) had reduced life span and elevated oxidative stress when compared with control. However, JB (0.25 and 1.0mg/kg diet) improved the motor function and also reduced the mortality rate of the flies exposed to LPS. It also restored the cellular antioxidant status and reduced acetylcholinesterase activity, accumulation of hydrogen peroxide as well as nitric oxide in Drosophila fed with LPS. JB also extended the longevity of the fliesrelative to control. The findings that JB improves motor function and extended the lifespan of Drosophila flies by boosting the antioxidant status and cholinergic function, suggest it might be helpful in delaying the onset of neuropsychiatric illnesses associated with the aging processes.

Influence of Classical Massage on Biochemical Markers of Oxidative Stress in Humans: Pilot Study.

Classical massage is one of the most popular forms of conservative treatment in various diseases. Despite the wide scope of research, the mechanisms of massage are not fully known and understood. Apart from the well-described effects on individual body systems, there are few scientific reports on the effects of massage on the human body at the subcellular level. The study was designed to assess changes in oxidative stress parameters in healthy volunteers after a single session of classical massage. 29 healthy volunteers aged 22.24 ± 3.64 participated in the study. Before and 30 minutes after the massage procedures, blood samples were taken by experienced personnel. Biochemical markers of oxidative homeostasis were assessed with highly specific methods for each parameter: oxidase ceruloplasmin, glutathione, malondialdehyde, glutathione peroxidase, glutathione S-transferase, and superoxide dismutase. The study demonstrates that massage therapy caused statistically significant decrease in the concentration of glutathione peroxidase (red blood cells) and increase in the level of glutathione peroxidase (plasma), superoxide dismutase, and malondialdehyde. In contrast, statistically significant changes in the hematocrit, glutathione, NO2-/NO3-, and oxidase ceruloplasmin were not observed. The results show that complex influence of classical massage therapy on human organism may be reflected in parameters of the oxidative stress. To understand this mechanism clearly, further research is needed.

A Systematic Review of Studies on Genotoxicity and Related Biomarkers in Populations Exposed to Pesticides in Mexico

In agricultural activities, pest control is essential, and the most effective method is the use of chemical agents that also represent an important source of exposure to potentially toxic compounds. Pesticides constitute a heterogeneous group of compounds designed specifically to control different pests. Besides measuring their levels or that of their metabolites in air, plasma, serum, blood, urine, etc., some studies reported increased DNA damage levels after occupational or environmental pesticides exposure, evidenced by several cytogenetic biomarkers such as chromosomal aberrations (CA), sister chromatid exchanges (SCE), micronuclei frequency (MN) together with other nuclear abnormalities (NA), alkaline comet assay, but also changes in oxidative stress parameters and miRNA levels. Single or combined, these techniques have also been used in genotoxic biomonitoring studies of workers occupationally exposed to pesticides in Mexico. Despite being a country with great agricultural activity and reported excessive pesticide use, genotoxic studies have been relatively few and, in some cases, contradictory. A review was made of the studies available (published until the end of 2020 on PubMed, Web of Science, Redalyc and Scielo, both in English and Spanish) in the scientific literature that evaluated occupational exposure of human samples to pesticides assessed with DNA damage and related biomarkers in Mexico.

Toxicological Impacts on Antioxidant Responses, Stress Protein, and Genotoxicity Parameters of Aluminum Oxide Nanoparticles in the Liver of Oreochromis niloticus.

The aim of this study was to determine the toxic effects of aluminum oxide nanoparticles (Al2O3 NPs) on oxidative stress, stress protein, and genotoxicity parameters in Oreochromis niloticus. Ninety-six-hour LC50 value of Al2O3 NPs was found as 52.4 ppm for O. niloticus. The fish were exposed to 2.6 ppm (5% of the 96-h LC50) and 5.2 ppm (10% of the 96-h LC50) for 3 days and 7 days. Various biochemical parameters, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) activities, glutathione (GSH), thiobarbituric acid reactive substance (TBARS), heat shock protein 70 (HSP70; stress protein), and genotoxicity biomarker 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, were determined. Results showed that antioxidant enzymes were significantly decreased in SOD, CAT, and GPx enzyme activity, but GST enzyme activity was significantly increased in 7 days. The oxidative stress parameters, GSH levels, were significantly decreased while 8-OHdG and TBARS levels were increased in 3 and 7 days. HSP70 levels were decreased in the concentrations of Al2O3 NPs and exposure times. Our results showed that as a result of changes in oxidative stress parameters, stress protein, and genotoxicity parameters, O. niloticus liver tissue is highly sensitive and toxic to aluminum oxide nanoparticle exposure.

Neuroprotective effect of paeonol in streptozotocin-induced diabetes in rats

BackgroundDiabetic neuropathy is one of the most common microvascular complication of diabetes. It is associated with neuronal dysfunction and pain. Paeonol is an important natural product reported for its antioxidant, anti-inflammatory and antidiabetic activities. AimThe present research was planned to study effect of paeonol in diabetic peripheral neuropathy in rats. MethodsDiabetes was induced in Sprague Dawley rats by using Streptozotocin (55 mg/kg, i.p.). After six weeks, diabetic animals were treated daily with paeonol at a dose of 50, 100 and 200 mg/kg for four weeks. At the end of the treatment, plasma glucose, mechanical allodynia, mechanical hyperalgesia, thermal hyperalgesia and nerve conduction velocities were recorded. Oxidative stress parameters were studied in sciatic nerve. Histopathology study of sciatic nerve, NF-κB and MCP-1 expression were also studied at the end of study. Key findingsPaeonol treatment significantly lowered the plasma glucose levels, mechanical allodynia, mechanical hyperalgesia and thermal hyperalgesia as compared to diabetic control group. Paeonol treatment also enhanced the motor and sensory nerve conduction velocity. Paeonol treated diabetic animals showed significant changes in oxidative stress parameters. Histopathology study indicated that paeonol treatment prevented the neuronal damage, lowered demyelination and leukocyte infiltration. NF-κB and MCP-1 expression was significantly decreased in sciatic nerve of diabetic animals treated with paeonol. SignificanceResults of the present study indicate that paeonol may be considered as effective option for management of diabetic neuropathy.

Commercial preparations of pesticides exert higher toxicity and cause changes at subcellular level in earthworm Eisenia andrei

BackgroundThe environmental impact of pesticides has been an increasingly discussed issue over the last decades. Constant usage of pesticides presents a burden for soil and causes a decrease in its health, including the negative effects on earthworms which are indicators for soil quality. The objective of this research was the assessment of the effects of two insecticides and two herbicides on the earthworm Eisenia andrei. Namely, the following active ingredients and respective commercial preparations were investigated: esfenvalerate (Sumialfa), thiacloprid (Calypso), dimethenamid-p (Frontier) and prosulfocarb (Filon). Lethal concentrations (48 h) of both active ingredient and commercial preparations were determined using the filter paper contact test.ResultsThe results showed that Calypso and Frontier were significantly more toxic than the active ingredient. Therefore, all further measurements were performed after exposure of earthworms to the commercial preparations of the pesticides. Specifically, several enzymatic biomarkers and multixenobiotic resistance activity were assessed. Additionally, a fluorescence-based assay for the determination of oxidative stress was established. Significant changes were detected for catalase, carboxylesterase and multixenobiotic activities after 48-h exposures. Also, a significant change in oxidative stress parameters could be observed for both Calypso and Frontier.ConclusionsThe obtained results show that commercial preparations can be more toxic than the active ingredients, and the formulations being distributed in the environment can affect earthworms on a molecular level already after short exposures. This emphasizes the importance of a more integrated eco-toxicological assessment of commercial pesticide preparations not to underestimate their effects on the environment.