Emerging issues in fisheries science by fisheries scientists.

The current epoch in fisheries science has been driven by continual advances in laboratory techniques and  increasingly sophisticated approaches to analysing datasets. We now have the scientific knowledge and tools to proactively identify obstacles to the sustainable management of marine resources. However, in addition to technological advances, there are predicted global environmental changes, each with inherent implications for fisheries. The 2023 symposium of the Fisheries Society of the British Isles called for "open and constructive knowledge exchange between scientists, stakeholders, managers and policymakers" (https://fsbi.org.uk/symposium-2023/), a nexus of collaborative groups best placed to identify issues and solutions. Arguably, the Centre of Environment, Aquaculture and Fisheries Science (Cefas) and their Scientific Advice for Fisheries Management (SAFM) Team sit at the centre of such a network. SAFM regularly engages with managers and stakeholders, undertakes scientific research, provides fisheries advice to the UK government, and are leading experts within the International Council for the Exploration of the Sea (ICES). As such, this paper is an opinion piece, linked to individual authors specialisms, that aims to highlight emerging issues affecting fisheries and suggest where research efforts could be focused that contribute to sustainable fisheries.

In vitro neurotoxic potential of emerging flame retardants on neuroblastoma cells in an acute exposure scenario.

Since 2004, some legacy flame retardants (FRs) were restricted or removed from the European markets due to their concern on human health. Both organophosphorus FRs (OPFRs) and novel brominated FRs (NBFRs) have replaced them because they are presumably safer and less persistent emerging FRs (EFRs) and their exposure is currently occurring in indoor environments at high levels. Little is known about the neurotoxic potential risk of these EFRs in humans. The present study was aimed at assessing the acute neurotoxicity potential of Tris(1, 3-dichloro-2-propyl)phosphate (TDCPP), triphenyl phosphate (TPhP), Bis(2-ethylhexyl)tetrabromophthalate (BEH-TEBP) and 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (EH-TBB) on human neuroblastoma cells (SH-SY5Y). SH-SY5Y were exposed to these EFRs at low concentrations -ranging 2.5-20 µM. during 2-24 h. We investigated viability, mitochondrial function, oxidative stress, inflammatory response, as well as neural plasticity and development. The results have demonstrated that selected EFRs (TDCPP, TPhP, EH-TBB and BEH-TBP) did not impair neural function on SH-SY5Y as acute response. To the best of our knowledge, this has been the first study focused on evaluating the neural affection of TPhP on SH-SY5Y cells and of EH-TBB and BEH-TBP on neural cells. We also assessed for the first time almost all endpoints after FR exposure on neural cell lines.

Effect of radiotherapy on the expression of cardiovascular disease-related miRNA-146a, -155, -221 and -222 in blood of women with breast cancer.

Breast cancer (BC) is one of the most important neoplasias among women. Many patients receive radiotherapy (RT), which involves radiation exposure of the thoracic zone, including the heart and blood vessels, leading to the development of cardiovascular disease (CVD) as a long-term side effect. The severity of CVD-related pathologies leads research on assessing novel CVD biomarkers as diagnostic, prognostic or therapeutic agents. Currently, the possible candidates include blood microRNAs (miRNAs). Previous studies have supported a role for miRNA-146a, -155, -221, and -222 in the progression of CVD. Our purpose was to evaluate the RT-induced modulation of the expression of these miRNAs in the blood of women with BC. Pre-RT control and post-RT blood samples were collected, and after miRNA isolation and reverse transcription, the levels of the selected miRNAs were measured by real-time PCR. Our results showed that miRNA-155 exhibited the lowest expression, while miRNA-222 exhibited the highest expression, followed by miRNA-221. The expression of each individual miRNA was positively correlated with that of the others both pre-RT control and post-RT and inversely correlated with age before RT. Furthermore, RT promoted the overexpression of the selected miRNAs. Their levels were also affected by CVD-linked clinical parameters, treatment and BC side. Modulation of the expression of the selected miRNAs together with other risk factors might be associated with the development of future cardiovascular pathologies. Further confirmatory studies are needed to assess their potential as possible biomarkers in the progression of or as therapeutic targets for RT-induced CVD in BC patients.

Effect of Radiation on the Expression of CVD-related miRNAs, Inflammation and Endothelial Dysfunction of HUVECs.

BACKGROUND/AIM: Radiotherapy (RT) can lead to cardiovascular disease (CVD). Evidence suggests that radiation modulates miRNA levels. Our purpose was to assess the acute response to radiation-induced modulation of the expression of miRNA-146a, miRNA-155, miRNA-221, and miRNA-222, inflammatory response and endothelial dysfunction on endothelial cells. MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were exposed to 2 Gy RT, and intracellular levels of selected miRNAs were measured by real-time polymerase chain reaction at 2 and 24 h. Cytokine and adhesion molecule release were also assessed. RESULTS: Results showed that 2 Gy significantly increased the expression of miRNA-221 and miRNA-222, and reduced the level of miRNA-155 after 2 h; whereas miRNA-146a and miRNA-155 were significantly overexpressed and miRNA-222 was significantly down-regulated at 24 h. Interleukin-8 and soluble vascular cell adhesion molecule 1 levels were not affected by the studied RT. CONCLUSION: RT at 2 Gy modulated expression of selected miRNAs by endothelial cells after 2 and 24 h, which might be related to CVD development in patients who receive RT.

In-vitro metabolomics to evaluate toxicity of particulate matter under environmentally realistic conditions.

In this pilot study three fractions of particulate matter (PM0.25, PM2.5-0.25, and PM10-2.5) were collected in three environments (classroom, home, and outdoors) in a village located nearby an industrial complex. Time-activity pattern of 20 students attending the classroom was obtained, and the dose of particles reaching the children's lungs under actual environmental conditions (i.e. real dose) was calculated via dosimetry model. The highest PM concentrations were reached in the classroom. Simulations showed that heavy intensity outdoor activities played a major role in PM deposition, especially in the upper part of the respiratory tract. The mass of PM10-2.5 reaching the alveoli was minor, while PM2.5-0.25 and PM0.25 apportion for most of the PM mass retained in the lungs. Consequently, PM2.5-0.25 and PM0.25 were the only fractions used in two subsequent toxicity assays onto alveolar cells (A549). First, a cytotoxicity dose-response assay was performed, and doses corresponding to 5% mortality (LC5) were estimated. Afterwards, two LC-MS metabolomic assays were conducted: one applying LC5, and another applying real dose. A lower estimated LC5 value was obtained for PM0.25 than PM2.5-0.25 (8.08 and 73.7 ng/mL respectively). The number of altered features after LC5 exposure was similar for both fractions (39 and 38 for PM0.25 and PM2.5-0.25 respectively), while after real dose exposure these numbers differed (10 and 5 for PM0.25 and PM2.5-0.25 respectively). The most metabolic changes were related to membrane and lung surfactant lipids. This study highlights the capacity of PM to alter metabolic profile of lung cells at conventional environmental levels.

Renal and hepatic effects following neonatal exposure to low doses of Bisphenol-A and 137Cs.

137-Cesium (137Cs) is one of the most important distributed radionuclides after a nuclear accident. Humans are usually co-exposed to various environmental toxicants, being Bisphenol-A (BPA) one of them. Exposure to IR and BPA in early life is of major concern, due to the higher vulnerability of developing organs. We evaluate the renal and hepatic effects of low doses of ionizing radiation (IR) and BPA. Sixty male mice (C57BL/6J) were randomly assigned to six experimental groups (n=10) and received a single subcutaneous dose of 0.9% saline solution, 137Cs and/or BPA on postnatal day 10: control, BPA (25 µg/kgbw), Cs4000 (4000 Bq 137Cs/kgbw), Cs8000 (8000 Bq 137Cs/kgbw), BPA/Cs4000 and BPA/Cs8000. At the age of two months, urines (24h) and blood samples were collected from animals of each group to determine biochemical parameters. Finally, kidneys and liver were removed to quantify DNA damage (8-OHdG), as well as to determine CYP1A2 mRNA expression. Data suggest that both BPA and 137Cs induced renal and liver damage evidenced by oxidative stress. However, when there is a co-exposure, it seems that there are compensatory mechanisms that may reverse the damage induced by each toxic itself. Notwithstanding, more studies are necessary to better understand the synergistic mechanisms behind.

Environmental exposure to low-doses of ionizing radiation. Effects on early nephrotoxicity in mice.

Nuclear accidents of tremendous magnitude, such as those of Chernobyl (1986) and Fukushima (2011), mean that individuals living in the contaminated areas are potentially exposed to ionizing radiation (IR). However, the dose-response relationship for effects of low doses of radiation is not still established. The present study was aimed at investigating in mice the early effects of low-dose internal radiation exposure on the kidney. Adult male (C57BL/6J) mice were divided into three groups. Two groups received a single subcutaneous (s.c.) doses of cesium (137Cs) with activities of 4000 and 8000Bq/kg bw. A third group (control group) received a single s.c. injection of 0.9% saline. To evaluate acute and subacute effects, mice (one-half of each group) were euthanized at 72h and 10 days post-exposure to 137Cs, respectively. Urine samples were collected for biochemical analysis, including the measurement of F2-isoprostane (F2-IsoP) and kidney injury molecule-1 (KIM-1) levels. Moreover, the concentrations of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA damage, were measured in renal tissue. Urinary excretion of total protein significantly increased at 72h in mice exposed to Cs4000. Uric acid and lactate dehydrogenase (LDH) decreased significantly at both times post-exposure in animals exposed to Cs8000. After 72h and 10d of exposure to Cs4000, a significant increase in the γ-glutamil transferase (GGT) and N-acetyl-ß-D-glucosaminidase (NAG) activities was observed. In turn, F2-IsoP levels increased -mainly in the Cs4000 group- at 72h post-exposure. Following irradiation (137Cs), the highest level of KIM-1 was corresponded to the Cs4000 group at 72h. Likewise, the main DNA damage was detected in mice exposed to Cs4000, mainly at 10d after irradiation. The alterations observed in several biomarkers suggest an immediate renal damage following exposure to low doses of IR (given as 137Cs). Further investigations are required to clarify the mechanisms involved in the internal IR-induced nephrotoxicity.

Radiotherapy for Graves' disease. The possible role of low-dose radiotherapy.

Immunomodulatory effects of low-dose radiotherapy (LD-RT) have been used for the treatment of several benign diseases, including arthrodegenerative and inflammatory pathologies. Graves' disease is an autoimmune disease and radiotherapy (RT) is a therapeutic option for ocular complications. The dose recommended in the clinical practice is 20 Gy (2 Gy/day). We hypothesized that lower doses (<10 Gy total dose, <1 Gy/day) could results in higher efficacy if we achieved anti-inflammatory and immunomodulatory effects of LD-RT. We review current evidence on the effects of RT in the treatment of Graves' disease and the possible use of LD-RT treatment strategy.

Exposure to low doses of 137cesium and nicotine during postnatal development modifies anxiety levels, learning, and spatial memory performance in mice.

Radiation therapy is a major cause of long-term complications observed in survivors of pediatric brain tumors. However, the effects of low-doses of ionizing radiation (IR) to the brain are less studied. On the other hand, tobacco is one of the most heavily abused drugs in the world. Tobacco is not only a health concern for adults. It has also shown to exert deleterious effects on fetuses, newborns, children and adolescents. Exposure to nicotine (Nic) from smoking may potentiate the toxic effects induced by IR on brain development. In this study, we evaluated in mice the cognitive effects of concomitant exposure to low doses of internal radiation (137Cs) and Nic during neonatal brain development. On postnatal day 10 (PND10), two groups of C57BL/6J mice were subcutaneously exposed to 137-Cesium (137Cs) (4000 and 8000 Bq/kg) and/or Nic (100 µg/ml). At the age of two months, neurobehavior of mice was assessed. Results showed that exposure to IR-alone or in combination with Nic-increased the anxiety-like of the animals without changing the activity levels. Moreover, exposure to IR impaired learning and spatial memory. However, Nic administration was able to reverse this effect, but only at the low dose of 137Cs.

Behavioral effects in mice of postnatal exposure to low-doses of 137-cesium and bisphenol A.

Bisphenol A (BPA) is the most important plasticizer used in many household products such as polycarbonate plastics or epoxy resins. Public and scientific concerns exist regarding the possibility that the neonatal exposure to BPA may contribute to neurobehavioral disorders. On the other hand, there is little information on the effects of low doses of ionizing radiation during critical phases of postnatal brain development, as well as the combination of radiation and environmental chemicals. In this study, C57BL/6J mice were exposed to low doses of internal radiation ((137)Cs), and/or BPA on postnatal day 10 (PND10). At the age of two months, animals were submitted to several tests to assess anxiety, activity, learning, and memory. Results showed that exposure to (137)Cs, alone or in combination with BPA, increased the anxiety-like of the animals without changing the activity levels. Animals exposed to (137)Cs showed impaired learning, and spatial memory, an impairment that was not observed in the groups co-exposed to BPA.

Human exposure to PBDE and critical evaluation of health hazards.

Polybrominated diphenyl ethers (PBDEs) are used in large quantities as flame-retardant additives in a number of commercial products. Biomonitoring data show that, in recent years, PBDE concentrations have increased rapidly in the bodies of wildlife and humans. Usually, PBDE levels in North America have been reported to be higher than those in Europe and Asia. Moreover, body burden of PBDEs is three- to ninefold higher in infants and toddlers than in adults, showing these last two age groups the highest levels of these compounds, due to exposure via maternal milk and through dust. Tetra-, Penta-, and Hexa-BDEs are the isomers most commonly found in humans. Based on studies on experimental animals, the toxicological endpoints of exposure to PBDEs are likely to be thyroid homeostasis disruption, neurodevelopmental deficits, reproductive changes, and even cancer. Experimental studies in animals and epidemiological observations in humans suggest that PBDEs may be developmental neurotoxicants. Pre- and/or postnatal exposure to PBDEs may cause long-lasting behavioral abnormalities, particularly on motor activity and cognition. This paper is focused on reviewing the current status of PBDEs in the environment, as well as the critical adverse health effects based on the recent studies on the toxic effects of PBDEs.

Neurobehavioral effects of concurrent exposure to cesium-137 and paraquat during neonatal development in mice.

As a result of nuclear power plants accidents such as Chernobyl or Fukushima, some people were exposed to external and internal ionizing radiation (IR). Human brain is highly sensitive to IR during fetal and postnatal period when the molecular processes are not completely finished. Various studies have shown that exposure to low doses of IR causes a higher incidence of cognitive impairment. On the other hand, in industrialized countries, people are daily exposed to a number of toxicant pollutants. Exposure to environmental chemicals, such as paraquat (PQ), may potentiate the toxic effects induced by radiation on brain development. In this study, we evaluated the cognitive effects of concomitant exposure to low doses of internal radiation ((137)Cs) and PQ during neonatal brain development. At the postnatal day 10 (PND10), two groups of mice (C57BL/6J) were exposed to (137)Cs (4000 and 8000 Bq/kg) and/or PQ (7 mg/kg). To investigate the spontaneous behavior, learning, memory capacities and anxiety, behavioral tests were conducted in the offspring at two months of age. The results showed that cognitive functions were not significantly affected when (137)Cs or PQ were administered alone. However, alterations in the working memory and anxiety were detected in mice exposed to (137)Cs combined with PQ.

Oxidative stress markers after a race in professional cyclists.

The aim was to determine the levels and activities of the oxidative stress markers in erythrocytes, plasma, and urine after a flat cyclist stage. Eight voluntary male professional trained-cyclists participated in the study. Exercise significantly increased erythrocyte, leukocyte, platelet, and reticulocyte counts. The exercise induced significant increases in the erythrocyte activities of catalase (19.8%) and glutathione reductase (19.2%), while glutathione peroxidase activity decreased significantly (29.3%). Erythrocyte GSSG concentration was significantly increased after exercise (21.4%), whereas GSH was significantly diminished (20.4%). Erythrocyte malondialdehyde levels evidenced a significant decrease 3 h after finishing the stage (44.3%). Plasma malondialdehyde, GSH and GSSG levels significantly decreased after 3 hr recovery (26.8%, 48.6%, and 31.1%, respectively). The exercise significantly increased the F2-isoprostane concentration in urine from 359 ± 71 pg/mg creatinine to 686 ± 139 pg/mg creatinine. In conclusion, a flat cycling stage induced changes in oxidative stress markers in erythrocytes, plasma, and urine of professional cyclists. Urine F2-isoprostane is a more useful biomarker for assessing the effects of acute exercise than the traditional malondialdehyde measurement.

Human dietary exposure to uranium in catalonia, Spain.

The purpose of this study was to determine the daily dietary intake of uranium (U) by the general population of Catalonia, Spain. Uranium concentrations were measured in foods widely consumed by the population living in that autonomous community. Food samples were randomly acquired in 12 representative cities of Catalonia. The dietary intake of U was estimated for various age-gender groups: children, adolescents, adults, and seniors. Fish and seafood was the food group showing the highest U concentrations (0.090 µg/g of fresh weight (fw)), followed by dairy products (0.044 µg/g fw). In contrast, the lowest U levels were found in oils and fats (0.003 µg/g fw), while in tubers and milk, U was not detected in any sample. The estimated dietary intake of U for a standard male adult of 70 kg body weight living in Catalonia was 15.48 µg/day. According to the age/gender of the population, the highest dietary intake of U corresponded to children (20.32 µg/day), while senior females was the subgroup with the lowest U intake (10.04 µg/day). Based on the tolerable daily intake established for U, the current dietary intake of this metal by the general population of Catalonia should not mean health risks for any of the different age/gender groups of consumers.

Oxidative stress as a mechanism underlying sulfasalazine-induced toxicity.

INTRODUCTION: Sulfasalazine (SASP) is a drug commonly used in the treatment of inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease (CD) and rheumatoid arthritis (RA). A high incidence of side effects limits therapy with this drug. Getting a wider knowledge of drug pharmacology, indications and side effects is essential to ensure the best possible clinical care, minimizing toxicity and inappropriate use. AREAS COVERED: This paper gives an overview of recent research about SASP and its main adverse effects, highlighting the mechanisms underlying them. To give an overview and comment on the data available so far on this topic, relevant literature was identified using a PubMed search of articles published up to December 2009. Search terms included: 'sulfasalazine', 'oxidative stress, 'renal effects', 'hepatotoxicity' and 'male fertility'. Original papers were reviewed and relevant citations from these articles were also considered. EXPERT OPINION: Although SASP and 5-aminosalicylic acid also scavenge ROS, which may account for some of their anti-inflammatory properties, the reaction with ROS may also generate toxic free radicals; hence, the ability of other antioxidants to suppress the toxicity of SASP in vivo. Further investigations, particularly about SASP mechanism, are still needed.

Environmental versus dietary exposure to POPs and metals: a probabilistic assessment of human health risks.

The human health risks derived from the multipathway/multipollutant exposure to various chemicals were assessed in an area with significant petrochemical activity (Tarragona, Catalonia, Spain). Environmental exposure to several Persistent Organic Pollutants (POPs) (PCDD/Fs, PCBs, PCNs, and PAHs) and metals (As, Cd, Cr, Hg, Mn, Pb, and V) was determined and compared with the dietary intake of these pollutants. The mean environmental exposure to organic pollutants ranged from 6.36 x 10(-6) ng WHO-TEQ kg(-1) day(-1) to 3.34 ng kg(-1) day(-1) for PCDD/Fs and PAHs, respectively. In turn, the minimum and maximum values of environmental exposure to metals corresponded to Cd (9.35 x 10(-8) mg kg(-1) day(-1)) and Mn (8.72 x 10(-5) mg kg(-1) day(-1)), respectively. Among the environmental exposure pathways, dermal absorption and soil ingestion were the most important pathways for POPs and metals, respectively. However, this exposure was notably lower than the dietary intake of these contaminants, with percentages of <2% for most of them. Considering cumulative effects, the current concentrations of micropollutants do not mean significant additional non-carcinogenic and carcinogenic human health risks. Notwithstanding, in order to consider the synergistic/antagonistic effects according to the target organ or mode-of-action, the development of alternative methodologies of risk assessment are necessary for a more accurate evaluation.

Effects of BDE-99 on hormone homeostasis and biochemical parameters in adult male rats.

In this study, we evaluated the effects of BDE-99 on hormone homeostasis, as well as in urinary and serum biochemical parameters of adult male rats. Animals (10 per group) received BDE-99 by gavage at single doses of 0, 0.6 and 1.2mg/kg. Forty-five days after BDE-99 exposure, urine and serum samples were collected for hormonal and biochemical analysis. Oxidative stress (OS) markers in erythrocytes, plasma and urine were also evaluated. Urinary excretion of total protein significantly increased following BDE-99 exposure, while lactate dehydrogenase (LDH), gamma-glutamil transferase (GGT), and N-acetylglucosaminidase (NAG) activities significantly decreased. Liver toxicity was evidenced by elevated serum activities of the enzymes glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT) and alkaline phosphatase (ALP). Following BDE-99 administration, OS markers in erythrocytes showed an increase in superoxide dismutase (SOD) activity, and a reduction in glutathione reductase (GR) activity. In urine, isoprostane levels increased after BDE-99 exposure. The hormonal analysis showed a significant decrease in testosterone and progesterone levels. These results support the hypothesis that BDE-99 interacts with hormonal response. Moreover, BDE-99 administration to adult male rats showed signs of renal and hepatic toxicity.

Effects of exposure to BDE-99 on oxidative status of liver and kidney in adult rats.

Little is known about the potential toxicity of polybrominated diphenyl ethers (PBDEs) on hepatic and renal tissues. In this study, we investigated the modifications in endogenous antioxidant capacity and oxidative damage in liver and kidney of rats by exposure to one of the most persistent PBDE congeners, the 2,2',4,4',5-pentabromodiphenyl ether (BDE-99). Adult male rats (10 per group) received BDE-99 by gavage at a single dose of 0, 0.6, and 1.2mg/kg body weight. Forty-five days after exposure, liver and kidney were removed and processed to examine the following oxidative stress (OS) markers: reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and thiobarbituric acid reactive substances (TBARS). In liver, BDE-99 significantly increased SOD activity, GSSG levels, and GSSG/GSH ratio, while GSH levels decreased. Moreover, CAT activity was only reduced at the highest BDE-99 dose. In kidney, CAT activity was significantly decreased, while GSSG/GSH ratio significantly increased following BDE-99 exposure at 1.2mg/kg body weight. Histological examination of tissues showed phagolysosomes in the kidneys of BDE-99-exposed rats. The results of this investigation suggest that acute oral BDE-99 exposure causes renal and liver impairment, being oxidative damage a potential mechanism for nephrotoxicity and hepatotoxicity.

Behavioral effects and oxidative status in brain regions of adult rats exposed to BDE-99.

Polybrominated diphenyl ethers (PBDEs) are used as flame retardants. Although developmental neurotoxicity of PBDEs has been already investigated, little is still known about their potential neurotoxic effects in adulthood. In this study, we assessed the oxidative damage in brain sections and the possible behavioral effects induced by exposure to 2,2',4,4',5-pentabromodiphenyl ether (BDE-99). Adult male rats (10/group) received BDE-99 by gavage at single doses of 0, 0.6 or 1.2mg/kg/body weight. Forty-five days after exposure, the following behavioral tests were conducted: open-field activity, passive avoidance and Morris water maze. Moreover, cortex, hippocampus and cerebellum were processed to examine the following oxidative stress (OS) markers: reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) and thiobarbituric acid reactive substances (TBARS). In cerebellum, BDE-99 significantly decreased SOD, CAT and GR activities at the highest BDE-99 dose. A decrease in CAT and SOD activities was also observed in cortex and hippocampus, respectively. In the behavioral tests, no BDE-99 effects were observed, while histopathological examination of the brain regions was normal. The current results show that the brain antioxidant capacity is affected by BDE-99 exposure, mainly in cerebellum. Oxidative damage could be a mechanism for BDE-99 neurotoxicity in adult rats.

Sulfasalazine induced oxidative stress: a possible mechanism of male infertility.

The mechanism of action of sulfasalazine (SASP) in male infertility is not well elucidated. For it, an oxidative stress-like mechanism inductor of infertility was hypothesized. Adult male Sprague-Dawley rats (20/group) were orally administered 0, 300, and 600mg SASP/kg body weight for 14 days. One-half of animals in each group remained an additional period of 14 days without treatment. SASP induced a significant decrease of superoxide dismutase (SOD) and glutathione reductase (GR) at the highest dose in both testis and epididymis. GR remained altered in these tissues within the recovery period. However, an increase in SOD was noted in epididymis. An increase in thiobarbituric acid-reactive substances (TBARS) was noted in all SASP-treated groups. In epididymis, catalase (CAT) significantly increased at 600mg/(kgday). These results suggest that SASP induces oxidative stress, which in turn might act as a possible mechanism of male-induced infertility.