Taurine alleviates heat stress-induced intestinal injury by inhibiting ROS-mediated endoplasmic reticulum stress in mice.

Acetylcholinesterase (AChE) is a key enzyme responsible for terminating cholinergic neurotransmission by hydrolyzing acetylcholine. While clinically approved AChE inhibitors such as donepezil, rivastigmine, and galantamine are used in the symptomatic treatment of Alzheimer’s disease and related dementias, little is known about the modulatory effects of common dietary compounds on AChE activity. In this study, we investigated the influence of creatine (CR) and taurine (TA)—two widely consumed nutritional supplements with reported neuroprotective and cognitive-enhancing properties—on AChE. Enzyme kinetics were evaluated using a modified Ellman’s method, and Lineweaver–Burk analyses revealed that both CR and TA act as competitive inhibitors. Calculated parameters (Km, Vmax), inhibition constants (Ki), and half maximal inhibitory concentrations (IC50) consistently indicated stronger potency for CR (IC50 = 0.0056 ± 0.00018 mM) compared to TA (IC50 = 0.0097 ± 0.00035 mM). To complement the experimental data, molecular docking was performed using two crystal structures of human AChE. Docking confirmed that both ligands preferentially occupy the active-site region in a manner consistent with competitive inhibition, with CR showing more favorable binding scores than TA. Although markedly weaker than clinical drugs, these findings provide the first biochemical and in silico evidence that CR and TA directly interact with AChE, suggesting subtle cholinergic modulation relevant to cognitive function and neuroprotection.

Introduction: Arsenic is a potent environmental toxin associated with male infertility. Taurine (TAU) has been demonstrated to regulate oxidative stress biomarkers and improve mitochondrial function. Materials and Methods: It evaluated the hypothesis that TAU could recover spermatogenesis dysfunction in an arsenic-treated rat model. Then, 24 adult male rats were challenged as follows (n=6/group) for 35 consecutive days: control (distilled water; gavage); 3 mg/l/day sodium arsenite; TAU (1000 mg/kg; 14) during arsenic exposure; and TAU during the study period. 24 h after the last treatment, animals were euthanized, serum samples were processed for assessing sex hormone levels, and testes were processed for weight, oxidative stress indices, histopathology, and RNA extraction for expression levels of autophagic marker genes. Results: Arsenic causes defective pathologic effects, and upregulates autophagic marker gene expression and production of free radicals. TAU exposure notably ameliorated the autophagy dysregulation through downregulation of the autophagic genes by inhibition of oxidative changes. Conclusion: This study presents a novel scientific approach to arsenic spermatogenesis dysfunction, attributed to TAU’s antioxidant activity.

Aeromonas hydrophila-induced bacterial sepsis is a major threat to aquaculture, characterised by excessive inflammation, ferroptosis (an iron-dependent lipid peroxidation-driven cell death) and oxidative damage, which collectively lead to high mortality. Taurine (TAU) and glutathione (GSH) have been demonstrated to have potential therapeutic efficacy against ferroptosis-associated pathologies through redox modulation. However, their combined effects and underlying mechanisms in alleviating A. hydrophila infection remain unclear. In this study, we investigated the protective roles of TAU, GSH and their combination invitro using yellow catfish (Pelteobagrus fulvidraco) macrophages and grass carp (Ctenopharyngodon idella) kidney (CIK) cells and invivo using yellow catfish challenged with A. hydrophila. The results showed that TAU and GSH, either alone or in combination, alleviated oxidative stress by significantly reducing reactive oxygen species (ROS) accumulation and inhibited nuclear factor-κB (NF-κB) pathway activation. This led to downregulated expression of pro-inflammatory cytokines (IL-1β and TNF-α) and upregulated anti-inflammatory cytokines (IL-10 and TGF-β), accompanied by alleviated ferroptosis. Invivo, dietary supplementation with TAU (10 g/kg) or GSH (350 mg/kg) alone improved survival rates (51.7% and 38.3%, respectively), reduced tissue bacterial loads and protected intestinal and hepatic tissues by preserving mucosal barrier function. However, the TAU + GSH combination unexpectedly decreased survival (28.3%) due to excessive immunosuppression (overproduction of IL-10 and TGF-β) and impaired mucosal barrier, which exacerbated pathogen colonisation. Together, our findings demonstrate that TAU and GSH alleviate A. hydrophila-induced oxidative stress by reducing mitochondrial ROS overproduction and disrupting the ROS/NF-κB signalling pathway, thereby attenuating inflammatory cytokine storms and ferroptosis. These results provide novel insights into the pathological mechanisms of bacterial sepsis in fish and develop sustainable strategies to improve disease resistance in aquaculture.

Cirrhosis is a chronic liver disease that is characterized by fibrosis and nodule formation that lead to alteration of the normal lobular organization of the liver. This study aimed to elucidate the antioxidant, antiapoptotic, and histological effects of taurine (TAU) and metformin (MET), both alone and in combination, in thioacetamide (TAA)-induced liver cirrhosis in rats. Liver cirrhosis was induced by injection of TAA (200 mg/kg/three times/week for 6 weeks). The treated groups were administered MET (200 mg/kg/day, p.o.), TAU (100 mg/kg/day, i.p.), and a combination of both for 5 weeks after TAA injection. The hallmarks of TAA-induced liver cirrhosis include increased oxidative stress, apoptosis, and decreased antioxidant levels in the liver tissue. This revealed that MET and TAU were used to treat TAA-induced liver damage. MET and TAU enhanced antioxidant systems by increasing superoxide dismutase, glutathione-S-transferase, and catalase and lowering malondialdehyde and nitric oxide levels. Furthermore, MET and TAU inhibited apoptosis through Bcl-2, Bax, and caspase-3 signaling pathways. These biochemical results were confirmed by liver histopathological analysis. Overall, posttreatment with MET and TAU demonstrated significant and synergizing protective effects against TAA-induced cirrhosis.

Heat stress induced by high temperature and humidity in southern China during summer reduce goat production efficiency and meat quality. Taurine (TAU), one of the most abundant amino acids in animal tissues, plays a vital role in alleviating heat stress and regulating energy metabolism through its involvement in glucose uptake and glycogen turnover. This study aimed to investigate the effects of rumen-protected (RP)-TAU on the meat quality, hepatic gluconeogenesis, and muscle energy metabolism of heat-stressed goats. During summer, twenty-four male crossbred Gan-xi goats (20.45 ± 2.95 kg) aged 5 months were randomly allocated to two groups treated with or without 0.4% RP-TAU (on a diet weight basis). After feeding for 60 days, six goats per treatment were slaughtered. Compared with the control group, RP-TAU supplementation significantly improved the growth performance of goats, as evidenced by increased final body weight, average daily gain, and average daily feed intake (p < 0.05). The goats in the RP-TAU group showed a reduced splenic index (p < 0.05), lower serum cortisol levels (0.05 < p < 0.1), and decreased muscle crude fat content (p < 0.01). Crucially, meat quality was improved with reduced hardness, gumminess, and chewiness (p < 0.05), indicating better textural properties. Nutritionally, RP-TAU supplementation modulated the muscle fatty acid profile, significantly reducing the concentrations of palmitic (a saturated fatty acid), palmitoleic (a monounsaturated fatty acid), and nervonic acids (p < 0.05), while cystine content was reduced (p < 0.05). RP-TAU supplementation significantly enhanced the muscle contents of glucose and glycogen, glycolytic potential, phosphofructokinase activity, and ATP level, while decreasing the pyruvate level and AMP/ATP ratio (p < 0.05). Gene expression analysis revealed the upregulation of GLUT4 and PYGM and the downregulation of GSK3β in muscle (p < 0.05). These results indicated that dietary supplementation of RP-TAU might be beneficial to improve stress resistance and meat quality by increasing muscle energy supply and glucose uptake in Gan-xi goats.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder affects motor and cognitive functions in patients. The main pathology of this illness is the loss of dopaminergic neurons in the substantia nigra which leads to locomotor impairment such as tremors, bradykinesia, and muscular rigidity. In late stages of PD, non-motor symptoms like cognitive deficits develop, affecting the life quality. Recent studies indicated that these non-motor symptoms are attributed to neuronal loss in the hippocampus and impaired neurotransmission, due to oxidative stress and neuroinflammation. This study aimed to evaluate the antioxidant and anti-inflammatory effects of Taurine (TRN) and taurine nanoparticles (TRN-NPs) and investigate their role in improving hippocampal neuronal survival and their synergistic effects with Sinemet tablets as a dopamine replacement, on rotenone-induced PD experimental mice model. The experiment involved 70 mice categorized into G1:control, G2:Sinemet (reference drug), G3:TRN-control, G4:TRN-NPs-control, G5:Rotenone (PD model), G6: Rotenone + Sinemet, G7:Rotenone + TRN, G8:Rotenone + TRN-NPs, G9:Rotenone + Sinemet + TRN and G10:Rotenone + Sinemet + TRN-NPs. At the experiment end, Behavioral parameter was defined using inverted screen test and various assessments. Neurotransmitters, oxidative stress biomarkers, pro-inflammatory cytokines, brain-derived neurotrophic factor (BDNF), micro-RNA 214, and micro-RNA 216a were evaluated. Treatment with TRN or TRN-NPs alone or with Sinemet alleviate oxidative stress, neuroinflammation and hippocampal neurodegeneration, enhance neurotransmission, neuronal survival and protection against cellular death. These results were confirmed by histological and immunohistochemical studies. The results suggest that TRN-NPs represent an innovative adjunct supplement to traditional dopaminergic therapies, improve neuroprotection, increased bioavailability, addressing current limitations in drug delivery and therapeutic efficacy thus opening up promising therapeutic approaches for PD management.

Background/Objectives: Thiamethoxam (TMX) is one of the most extensively utilized insecticides of the neonicotinoid family; however, its application is associated with notable toxic effects on multiple organs of mammals. Our purpose was to explore the potential hepatoprotective effect of taurine (TAU) and/or gallic acid (GA) against TMX-induced liver damage, with an emphasis on their role in regulating SIRT-1/PGC-1α, NF-κB/iNOS, and p53/Bax/caspase-3 pathways. Methods: Rats were assigned to seven groups (n = 6) and gavaged daily for 28 days with saline (control group), TAU at 50 mg/kg, GA at 20 mg/kg, TMX at 78.15 mg/kg, TMX + TAU, TMX + GA, and TMX + TAU + GA. Results: The findings revealed that TAU and/or GA attenuated TMX-induced liver injury, as demonstrated by the restoration of hepatic performance hallmarks and histological structure. TAU and GA mitigated TMX-mediated oxidative stress and boosted the antioxidant defense mechanism by upregulating the transcription levels of SIRT-1, PGC-1α, Nrf2, and HO-1. Moreover, TAU and GA suppressed TMX-associated inflammatory response by increasing IL-10 concentration and lowering the levels of NF-κB, IL-1β, and iNOS; the mRNA levels of NLRP3; and TNF-α immunoexpression. Both compounds, individually or concurrently, exerted an anti-apoptotic effect in TMX-treated rats, evidenced by increased Bcl-2 expression and reduced p53 mRNA level, Bax expression, and caspase-3 concentration. Conclusions: TAU and/or GA may be regarded as promising remedies that can alleviate TMX-induced hepatotoxicity by activating SIRT-1/PGC-1α signaling and abolishing inflammation and apoptosis.

Effect of methionine replacement with taurine on the performance and antioxidative capacity of broiler

Ultrasound-responsive taurine lipid nanoparticles attenuate oxidative stress and promote macrophage polarization for diabetic wound healing.

Abstract Objectives Letrozole (LTZ), an aromatase inhibitor, is associated with significant side effects such as uterine toxicity. This study investigated the potential of hesperidin (HSP) and taurine (TAU), both natural antioxidant molecules, to mitigate LTZ-induced uterine toxicity. Methods A total of 48 female rats were divided into six groups and treated orally for 30 days as follows: Control (sham), LTZ (1 mg/kg), HSP (100 mg/kg), TAU (100 mg/kg), LTZ+HSP, and LTZ+TAU. Histopathological, gene expression, and biochemical analyses were conducted on uterine tissues and serum samples. Results LTZ caused a significant decrease in serum IL-1β, IL-6, estradiol, and FSH levels (p&lt;0.05). It reduced SOD, CAT activities, and GSH levels while increasing tissue MDA levels. Additionally, it led to a significant increase in Bax, caspase-3, COX-2, iNOS, and TNF-α gene expression. HSP and TAU did not significantly alter hormone levels (p&gt;0.05). However, HSP significantly reduced oxidative stress (p&lt;0.05), decreased the expression of genes related to apoptosis and inflammation (p&lt;0.05), and significantly lowered serum cytokine levels while increasing the expression of anti-apoptotic genes. Both HSP and TAU mitigated LTZ-induced cystic dilatation and hyperemia in the uterine glands. TAU did not significantly affect IL-1β and IL-6 levels or the expression of apoptosis-related genes (p&gt;0.05). Although TAU exhibited effects similar to HSP in certain parameters, its protective efficacy was comparatively less pronounced. Conclusions The results suggest that HSP is a promising agent for mitigating LTZ-induced uterine toxicity. However, further studies with different doses and application protocols are required to more definitively elucidate the potential effects of TAU.

Background: Diabetes mellitus poses a significant health challenge worldwide. Oxidative stress, altered lipid profile, and inflammation are linked to diabetic complications. Objective: This work aimed to assess the effects of taurine (TAU) in alloxan (ALX)-induced diabetes in rats, evaluating its antihyperglycemic, antidyslipidemic, antioxidant, and anti-inflammatory effects. In addition, evaluating the effect of TAU on hepatic, renal, and cardiac complications. Materials and Methods: Fifty rats were divided into four groups, control, TAU, ALX, and ALX + TAU. At the end of the experiment, blood and tissue were collected and subjected to serum glucose, insulin, lipid profile, liver enzyme, creatinine, urea detection, oxidative-antioxidant parameters evaluation, inflammatory, anti-inflammatory cytokines detection, and histological evaluation. Results: Experimental results demonstrated that TAU effectively mitigated hyperglycemia, dyslipidemia, oxidative stress, and inflammatory conditions induced by ALX. TAU treatment improved serum glucose and insulin levels, restored lipid profiles, enhanced antioxidant enzyme activities, and reduced lipid peroxidation. In addition, TAU ameliorated hepatic and renal function alterations preserved histological architecture in the pancreas, liver, kidney, and heart tissues, and modulated inflammatory responses by diminishing the inflammatory mediators interleukin-6 (IL-6) and tumor necrosis factor-α while augmenting the anti-inflammatory mediator IL-10. Conclusions: TAU exerts a therapeutic effect on ALX-induced hepatic, renal, and cardiac diabetic complications by lowering blood glucose levels, augmenting insulin secretion, ameliorating dyslipidemia, preserving the oxidative-redox balance, and boosting antioxidant activity. TAU has also an anti-inflammatory impact.

ABSTRACT Taurine (TAR) intricately mediates a plethora of physiological processes. This investigation aimed to elucidate the impact of TAR (50, 100, 150, and 200 mg L−1) seed priming on redox homeostasis, glutathione metabolism, photosynthetic efficiency, osmotic adjustment and nutrient acquisition in pea plants subjected to 100 mm salinity of neutral (NaCl and Na2SO4) and alkaline (Na2CO3) salts. Salinity diminished growth, chlorophyll, and photosynthetic efficiency alongside a concurrent rise in reactive oxygen species (ROS), lipid peroxidation, and relative membrane permeability. Seed priming with 150 mg L−1 TAR efficiently enhanced growth by reducing oxidative damage to plants under salinity. Taurine enhanced leaf relative water content through osmotic adjustment facilitated by the induced accumulation of proline, glycine betaine, soluble sugars, and total free amino acids. Taurine increased the levels of antioxidant compounds and the activities of enzymes, which assisted in the detoxification of ROS and methylglyoxal. Taurine maintained chlorophyll integrity and enhanced photosynthetic efficiency by alleviating oxidative stress. Taurine diminished Na content, which improved the acquisition of essential nutrients under the salinity of neutral and alkaline salts. The results suggest that TAR has a potential role in maintaining ion homeostasis, crucial for enhancing pea tolerance to salt stress.

Taurine (TAU) and creatine (Cr) are common ergogenic aids used by athletes to enhance performance; however, the effect of their combined supplementation, and on recovery in high temperature and humidity environments, has not been studied. Combined TUA and Cr will have greater effect on physiological indicators and repetitive sprint performance recovery after exhaustive exercise under hot and humid conditions than single supplementation or placebo. Single-blind crossover randomized controlled study. Level 2. Participants (12 sports students) were assigned randomly to 1 of 4 supplementation intervention groups: placebo (P), taurine (T), creatine (C), or taurine + creatine (T+C). Exercise protocol included exhaustion tests and repeated sprinting exercises were conducted in a laboratory environment at 35 °C/65% relative humidity. Heartrate, blood lactate (BLa), tympanic temperature, thermal sensation, and rating of perceived exertion were monitored throughout. Heartrate variability, time to exhaustion (TTE), reaction time, and countermovement jump (CMJ) height were tracked before and after exhaustion exercise and before sprint exercise. TTE was significantly higher in the T+C group than in the P group (P = 0.04). BLa and tympanic temperature increased rapidly in all 4 conditions, then decreased gradually, and T group peak values were higher than those of P group (P = 0.04; P < 0.01). CMJ decreased in the C and T+C groups (P = 0.04; P = 0.04) after exhaustive exercise, unlike other groups (P > 0.05). Indicators of repeated sprint exercise, peak power, mean power, and power decrement showed a decreasing trend within groups but no difference between groups (P > 0.05). In this small student group, under hot and humid conditions, T+C supplementation significantly enhanced TTE. TAU, Cr, and their combined supplementation do not significantly improve repeated sprint performance after exhaustive exercise under hot and humid conditions.

From 1 January 2024, the sale of energy drinks (EDs) containing caffeine (CAF) and taurine (TA) was legally banned in Poland for minors (under age 18 years). EDs pose a significant public health concern, with their consumption steadily rising among young people globally. These beverages are rich in CAF, sugar, and other stimulants, making them particularly attractive to adolescents seeking energy boosts during physical or mental exertion. ED consumption patterns vary based on sociodemographic factors, with gender playing a notable role. The consumption of EDs by children and adolescents has been linked to adverse health effects and risky behaviors, potentially affecting their overall well-being. Excessive ED consumption is a widespread issue, prompting numerous countries to implement regulatory measures, such as sales restrictions for under those under age 18 years, warning labels, and mandatory disclosure of CAF content. This review examines ED consumption among people under age 18 years in Poland, focusing on the associated health and regulatory challenges of the newly introduced sales prohibition. Despite the growing popularity of EDs among young people, Poland lacks systematic studies on their consumption, particularly among children, adolescents, and young adults. Beyond legal restrictions, coordinated health policies and education about the risks of ED consumption and natural alternatives are crucial to addressing this issue. This article aims to review the background to the reasons for the ban of sale of energy drinks to young people in Poland from January 2024.

ABSTRACT Taurine (TAU) has recently been found to have an impactful role in regulating plant responses under abiotic stresses. This study presented the comparative effects of TAU seed priming and foliar spray application on chickpea plants exposed to hexavalent chromium. Taurine priming and foliar applications (1.6 and 2.4 mM) notably modulated morpho-physiological and biochemical responses of plants under Cr(VI) stress. Plants subjected to 25 mg kg−1 soil Cr in the form of potassium dichromate (K2Cr2O7) displayed a significant reduction in growth, chlorophyll, and uptake of essential nutrients (N, K, P, and Ca). Cr(VI) toxicity also resulted in a notable increase in osmolyte accumulation, lipid peroxidation, relative membrane permeability, ROS generation, antioxidant enzyme activities, antioxidant compounds, endogenous Cr levels, and aerial Cr translocation. Taurine abridged lipoxygenase activity to diminish lipid peroxidation owing to the overproduction of ROS initiated by a higher Cr content. The acquisition and assimilation of essential nutrients were augmented by the TAU-related decrease in leaf and root Cr levels. Consequently, TAU enhanced growth by mitigating oxidative damage, reducing Cr content in the aerial parts, and reinforcing the activities of antioxidant enzymes. Compared to foliar spray, TAU seed priming has demonstrated superior efficacy in mitigating Cr phytotoxicity in plants.

Taurine (TAU) has been shown to improve time to exhaustion (TTE) and fat oxidation during exercise; however, no studies have examined the effect of acute TAU supplementation on maximal fat oxidation (MFO) and related intensity to MFO (FATmax). Our study aimed to investigate the effect of acute TAU supplementation on MFO, FATmax, VO2peak, and TTE. Eleven recreationally trained male endurance runners performed three incremental running tests. The first visit included a familiarization to the test, followed by two subsequent visits in which exercise was performed 90min after ingestion of either 6-g TAU or placebo (PLA) using a triple-blind randomized crossover design. There was no effect of TAU on MFO (p = .89, d = -0.07, TAU: 0.48 ± 0.22g/min; PLA: 0.49 ± 0.15g/min or FATmax (p = .26, d = -0.66; TAU: 49.17 ± 15.86 %V˙O2peak; PLA: 56.00 ± 13.27 %V˙O2peak). TTE was not significantly altered (TAU: 1,444.8 ± 88.6s; PLA: 1,447.6 ± 87.34s; p = .65, d = -0.04). TAU did not show any effect on V˙O2peak in comparison with PLA (TAU: 58.9 ± 8.4ml·kg-1·min-1; PLA: 56.5 ± 5.7ml·kg-1·min-1, p = .47, d = 0.48). However, V˙O2 was increased with TAU at most stages of exercise with large effect sizes. The acute ingestion of 6 g of TAU before exercise did not enhance MFO, FATmax, or TTE. However, it did increase the oxygen cost of running fixed intensities in recreationally trained endurance runners.

Tartrazine (TZ) is an anionic azo dye widely used to color food products, pharmaceuticals, and cosmetics; however, its harmful effects on the kidneys are still unclear and need to be confirmed. Meanwhile, taurine (TA) is a natural antioxidant amino acid that can provide protection against various forms of glomerulonephritis. Our aim was to study the structural, and biochemical effects of TZ on the kidney and evaluate the potential protection provided by taurine. We used 28 adult male albino rats equally divided into 4 groups. The control group did not receive TZ or TA. The TA group received 100 mg/kg/day of TA. The TZ group received 100 mg/kg/day of TZ dissolved in distilled water. The TZ/TA group received both TZ and TA. Animal blood samples were obtained to estimate blood urea, creatinine, and random glucose levels. Kidneys samples were examined for structure as well as oxidative enzymes and kidney injury molecule 1 (KIM-1). Compared to the control group, the TZ group showed hyperglycemia, increased markers of oxidative stress, and shrunken, lobulated glomeruli with mesangial expansion, pyknosis, and vacuolation in the tubular lining. There was also strong immunoreactivity for PCNA and caspase-3, a thickened glomerular capillary basement membrane lacking fenestrations, swollen mitochondria with destructed cristae, and increased expression of the KIM-1. In the TZ/TA group, the convoluted tubules mostly retained the normal histological structure, but some tubules still showed a wide lumen and nuclear pyknosis of lining cells. Oxidative markers and random blood glucose levels were significantly reduced. TZ is suggested to cause adverse kidney effects in rats, including kidney injury and structural changes, which can be mitigated by co-administration with TA.

This study evaluated the effect of four attractants on the growth performance, antioxidant capacity, immunity, and histology of largemouth bass larvae (Micropterus salmoides). A total of 75,000 larvae (~1.25 mg) were randomly divided into 15 tanks (five groups with three replicates), with 5000 larvae per tank. The experimental diets were isonitrogenous (54.45% crude protein) and isolipidic (13.20% crude lipid), including a control group (CON, no attractants), taurine (TAU) group (8 g/kg, trimethylamine oxide (TMAO) group (0.25 g/kg), dimethyl‐β‐propiothetin (DMPT) group (5 g/kg), and nucleotides (NTs) group (0.8 g/kg). The feeding trial was conducted in tanks (40 cm × 60 cm × 80 cm) for 21 days. The larvae were fed with Artemia three times daily for 7 days. The 21‐day feeding trial started on the 8th day, alternated with feed six times daily from the 8th to 15th day, then fully transitioned to experimental diets with adjusted feed sizes. The results showed that TAU, DMPT, and NT groups significantly increased the final body weight (FBW), weight gain (WG), and specific growth rate (SGR) (p < 0.05), while TMAO, DMPT, and NT groups significantly increased the survival rate (SR) (p < 0.05), compared with the CON group. During the air stress challenge, compared with the CON group, all treatments significantly prolonged survival time (p < 0.05). Compared with the CON group, the TAU and NT groups significantly increased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) content, and decreased the malondialdehyde (MDA) content (p < 0.05), and the total antioxidant capacity (T‐AOC) in the NT group was significantly increased (p < 0.05). All treatments significantly increased the activities of acid phosphatase (ACP) and alkaline phosphatase (AKP; p < 0.05). Compared with the CON group, the histological intestine indicated that all treatments significantly increased the intestinal fold height and decreased the muscular layer thickness, crypt depth, and fold width (p < 0.05); the histological liver indicated that the TMAO and NT groups could improve liver cells. In conclusion, all attractants exerted positive effects on largemouth bass larvae, with TAU, DMPT, and NT demonstrating significant growth enhancement associated with improved antioxidant capacity, immune response, and tissue histology. Further research is needed to clarify mechanisms and optimal doses.

Background: Chemotherapy involves the use of chemical agents to kill cancer cells, but it can also harm healthy, rapidly growing cells in the body. 5-fluorouracil (5-FU) induces tissue damage through oxidative stress and impaired male reproductive activity. The use of antioxidants appears to mitigate the harmful effects caused by 5-FU. Objectives: This study evaluated the potential protective effects of taurine (TAU) against 5-FU-induced testicular toxicity in male rats. Methods: Thirty-five healthy adult male Wistar rats (200 - 250 g, 6 - 8 weeks old) were randomly divided into five groups: Control, 20 mg/kg 5-FU, and 50, 100, and 200 mg/kg of TAU co-administered with 20 mg/kg 5-FU. Treatments were administered intraperitoneally for 14 consecutive days. Serum endocrinological analyses, as well as testicular biochemical and histomorphometric studies, were performed on the different groups. Results: Testis and epididymis weights significantly decreased (P &lt; 0.001) in male rats treated with 5-FU. Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T4) were significantly lower (P &lt; 0.05) in 5-FU-treated rats. Testicular tissue of 5-FU-treated rats exhibited significantly reduced activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) (P &lt; 0.001) and increased levels of malondialdehyde (MDA) (P &lt; 0.001). Co-administration of TAU significantly improved germinal epithelium height (GEH) and seminiferous tubule diameter (STD) (P &lt; 0.001) in 5-FU-treated rats. Additionally, TAU co-administration significantly improved oxidative status and reproductive parameters in 5-FU-treated rats. Conclusions: These findings suggest that TAU has the potential to prevent 5-FU-induced testicular oxidative toxicity and restore suppressed reproductive parameters in male rats.