Early life trauma/stress is associated with behavioral abnormalities, memory impairment, and long-term neurodevelopmental alterations. Brain-derived neurotrophic factor (BDNF) and its associated signaling pathways have been investigated for their roles in linking stress with neurological complications. Taurine (TAU), the most abundant non-protein amino acid in the body, is known for its significant effects on the central nervous system (CNS); however, its precise mechanisms of action are vague. This study aimed to investigate the effects of TAU on the BDNF/TrkB/ERK1/CREB signaling pathway in the hippocampus and its impact on memory, cognitive deficits, and depression-like behaviors in the maternal separation and early weaning (MSEW) model. The amino acid TAU was administered to mouse offspring (50 and 100 mg/kg, s.c., started on the post-natal day; PND = 6) of the control and MSEW model. Behavioral tests revealed significant memory impairments and depression-like behavior during puberty, with no significant changes in memory indices observed in adult offspring. Notably, TAU treatment significantly ameliorated memory impairments and reduced cognitive disorder and depression markers during puberty (PND = 35). In the MSEW group, the expression/levels of BDNF, TrkB, ERK1, and CREB were markedly downregulated during puberty, while no significant changes were detected in adult animals (PND = 85). Notably, the TAU administration significantly upregulated components of the BDNF/TrkB/ERK1/CREB signaling pathway in both juvenile and adult mice. These findings suggest that TAU may have therapeutic potential in mitigating early-life trauma-induced neurodevelopmental deficits by modulating the BDNF/TrkB/ERK1/CREB pathway. Given the critical role of this signaling pathway in various CNS disorders, further investigations are warranted to explore the effects of TAU in the CNS and to elucidate its potential as a candidate for further investigation in stress-related neurodevelopmental and neurobehavioral disorders.

In three patients with aluminum phosphide poisoning, intravenous dihydroxyacetone (DHA) was added to standard supportive care. Improvement in metabolic acidosis and hemodynamic status was temporally associated with DHA administration. Controlled studies are needed to determine efficacy and safety.

Substance withdrawal syndromes pose significant challenges in addiction treatment, often leading to poor treatment adherence and high relapse rates. This review evaluates metformin's potential as a therapeutic option for substance withdrawal syndromes, focusing on its mechanisms (AMPK activation, neurotransmitter modulation, gut microbiome effects) and clinical implications. Proposed mechanisms of action, including the involvement of signaling pathways, neurotransmitter regulation, and gut microbiome modulation, are also discussed. The study also highlights key areas requiring further investigation, such as the need for well-designed clinical trials, exploration of metformin dosage and treatment duration, and a deeper understanding of the specific molecular pathways underlying metformin's impact on withdrawal syndromes. Preclinical and clinical evidence suggest that metformin alleviates withdrawal symptoms and reduces relapse risk, but further research is needed to optimize dosing and validate efficacy. Overall, this review supports metformin's potential as a promising therapeutic option for managing substance withdrawal syndromes, offering improved treatment outcomes and reduced relapse rates and vulnerabilities.

[This corrects the article DOI: 10.1016/j.livres.2020.12.001.].

Aim of the study:Cholestasis is characterized by impaired bile flow from the liver to the small intestine. Beyond liver damage, cholestasis significantly affects other organs, particularly the kidneys, causing a condition known as cholemic nephropathy (CN). Sildenafil is a phosphodiesterase type 5 (PDE5) enzyme inhibitor with a wide range of pharmacological effects. Several studies have described the nephroprotective properties of sildenafil. Material and methods:Rats underwent bile duct ligation (BDL) surgery to induce cholestasis and CN. Afterward, BDL animals received sildenafil (5, 10, and 20 mg/kg/day, i.p., for 14 consecutive days). Urine, blood, and kidney samples were collected for further evaluation. Results:Elevated levels of blood urea nitrogen (BUN) and creatinine (Cr) and urinalysis revealed renal injury in this model (p < 0.001). Oxidative stress markers, including depleted antioxidant capacity, increased ROS formation, lipid peroxidation, and protein carbonylation, were evident in the kidneys of BDL rats (p < 0.001). Moreover, the activity of enzymatic antioxidant systems (CAT, SOD, GR, and GPx) was also significantly decreased in the kidney of BDL animals (p < 0.001). Tissue pro-inflammatory cytokines (TNF-a, IL-6, and IL-1b) were also considerably higher in the kidney of cholestatic rats (p < 0.001). Renal histopathological changes in BDL animals included inflammatory cell infiltration, tubular atrophy, necrosis, significant fibrotic changes, and cast formation. It was found that sildenafil significantly reduced pathological changes, mitigated oxidative stress biomarkers, and suppressed inflammation in the kidneys of BDL animals. The nephroprotective effects of sildenafil were not dose-dependent in the current study. Conclusions:The data obtained from this study revealed that sildenafil could significantly protect against renal damage in cholestasis. The effect of sildenafil on oxidative stress and the inflammatory response plays an essential role in its nephroprotective mechanisms.

Hepatic encephalopathy (HE) is a clinical situation that refers to neurological complications of liver failure and hyperammonemia. Ammonia (ammonium ion in biological fluids; NH4+) is the primary culprit of brain injury in HE. Although the precise mechanism of NH4+-induced neurotoxicity is far from clear, it has been well-established that this chemical can induce significant oxidative stress in the brain. At subcellular levels, mitochondria are critical targets for NH4+ cytotoxicity. Therefore, potential therapeutic approaches in HE targeted oxidative stress and mitochondrial impairment. Hence, developing convenient, reliable, and reproducible methods is crucial for assessing and monitoring therapeutic interventions in HE. In the current protocol, an animal model of acute HE is described. Then, techniques for evaluating oxidative stress biomarkers in the brain, isolating brain mitochondria, and assessing mitochondrial indices are outlined.

Acute kidney injury (AKI) is a significant clinical problem associated with high morbidity and mortality. Unilateral ureter obstruction (UUO) is a well-established model for studying the pathophysiology of AKI. L arginine (ARG), a precursor of nitric oxide, has been shown to possess renoprotective properties. This study aims to investigate the protective effects of ARG in an animal model of UUO-induced AKI. Male BALB/c mice were randomly allotted into sham-operated, UUO, and UUO + L-Arginine. UUO was surgically induced by ligating the left ureter. The treatment group received ARG (100, 250, and 500 mg/kg/day) intraperitoneally for seven days post-UUO surgery. Renal function was assessed by measuring plasma creatinine (Cr) and blood urea nitrogen (BUN) levels. Mitochondrial function was evaluated by determining mitochondrial membrane potential, dehydrogenases activity, and mitochondrial swelling. Oxidative stress markers, including ROS formation, lipid peroxidation, protein carbonylation, and tissue antioxidant capacity, were also measured in the kidney tissue. UUO led to significant renal dysfunction, as evidenced by increased serum Cr and BUN levels (P<0.001). Mitochondrial dysfunction was indicated by decreased mitochondrial dehydrogenase activity, mitochondrial depolarization, and increased mitochondrial swelling (P<0.001). Additionally, UUO-induced oxidative stress was demonstrated. It was found that ARG treatment significantly improved renal function by modulating mitochondrial function and decreasing oxidative stress markers (P<0.05). These findings suggest that ARG may have therapeutic potential in managing AKI by preserving mitochondrial function and reducing oxidative damage.

Acute pancreatitis (AP) is a severe inflammatory disorder with a significant risk of mortality. However, restricted pharmacological treatments are available against this complication. Carnosine is an endogenous dipeptide with various pharmacological effects, including antioxidative and anti-inflammatory properties. The current study was designed to evaluate the impact of carnosine in an experimental model of AP. For this purpose, mice received arginine (two 4 g/kg doses, one-hour intervals, i.p) to induce AP. Then, animals received carnosine (50, 250, and 500 mg/kg, i.p). Serum levels of amylase, lipase, and glucose were significantly increased (P<0.001) in the current AP model. Moreover, alterations in oxidative stress biomarkers in the pancreas, including ROS formation, decreased antioxidant capacity, lipid peroxidation, and glutathione depletion, were detected in the AP group (P<0.001). A significant increase in the pancreatic level of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) was also evident in the l-arginine-treated mice (P<0.001). The major pancreatic tissue histopathological changes in the current AP model were the infiltration of inflammatory cells to the pancreas tissue, fluid accumulation, and acinar cell vacuolization/necrosis (P<0.05). Carnosine significantly reduced serum biomarkers of pancreas injury, alleviated oxidative stress, decreased pro-inflammatory cytokine levels, and improved histopathological changes in the pancreas of mice with AP (P<0.001). These findings suggest that carnosine is a protective agent in pancreatitis, with its antioxidative and anti-inflammatory properties playing a pivotal role in its mechanisms of action. Further research is needed to confirm these protective effects in clinical studies and assess carnosine safety in AP.

BACKGROUND:Taurine (TAU) is the most abundant non-protein amino acid in the central nervous system (CNS). However, the molecular mechanism of TAU in the CNS is still poorly understood. Meanwhile, disruption in mitochondrial dynamics is evident in CNS disorders. This study aimed to investigate the effect of TAU on mitochondrial dynamics. METHODS:TAU (0.25, 0.5 and 1% in drinking water) was administered to young mice for six months. Several memory/cognition parameters and indices of anxiety/depression were assessed. Meanwhile, various mitochondrial indices and the expression/activity of genes involved in mitochondrial biogenesis and dynamics (Akt, CREB, NRF1, TFAM, PGC-1α, Mfn1, Mfn2, UCP2, PINK1, OPA1, Drp1 and Fis1) were examined. RESULTS:TAU significantly enhanced memory performance, suppressed anxiety and depression-like behaviour, increased mitochondrial biogenesis/dynamics and improved mitochondrial indices. It should be mentioned that there was no significant difference between different concentrations of TAU in changing most brain mitochondrial dynamic biomarkers in the current study. CONCLUSIONS:These findings offer more insights into the molecular mechanism for TAU's action in the CNS. However, there is a need for further research to confirm these effects in humans. Overall, this study suggests the potential application of TAU in various neurological disorders and the need for clinical studies on the effects of this amino acid in the brain.

Taurine (TAU) is a sulfur-containing amino acid abundantly found in the human body. Endogenously, TAU is synthesized from cysteine in the liver. However, newborns rely entirely on TAU's dietary supply (milk). There is no investigation on the effect of long-term TAU administration on next-generation neurological development. The current study evaluated the effect of long-term TAU supplementation during the maternal gestational and litter weaning time on several neurological parameters in mice offspring. Moreover, the effects of TAU on mitochondrial function and oxidative stress biomarkers as plausible mechanisms of its action in the whole brain and hippocampus have been evaluated. TAU (0.5 % and 1 % w/v) was dissolved in the drinking water of pregnant mice (Day one of pregnancy), and amino acid supplementation was continued during the weaning time (post-natal day; PND = 21) until litters maturity (PND = 65). It was found that TAU significantly improved cognitive function, memory performance, reflexive motor activity, and emotional behaviors in F1-mice gener-ation. TAU measurement in the brain and hippocampus revealed higher levels of this amino acid. TAU and ATP levels were also significantly higher in the mitochondria isolated from the whole brain and hippocampus. Based on these data, TAU could be suggested as a supplement during pregnancy or in pediatric formula. The effects of TAU on cellular mitochondrial function and energy metabolism might play a fundamental role in the positive effects of this amino acid observed in this investigation.

Background: Cholestasis is a multifaceted disease that influences not only the function of the liver but also affects many other organs. In this context, cholestasis-induced lung injury is a significant clinical complication. Unfortunately, there is no precise therapeutic option against cholestasis-associated lung injury. It has been revealed that oxidative stress and inflammatory response play a role in cholestasis-induced pulmonary damage. Sildenafil is a phosphodiesterase enzyme inhibitor used in the management of erectile dysfunction. Meanwhile, several experiments revealed the effects of sildenafil on oxidative stress and inflammation. This study aimed to evaluate the effect of sildenafil on cholestasis-induced oxidative stress and inflammation in cholestasis-induced lung injury. Methods: Rats underwent bile duct ligation (BDL) to induce cholestasis. Bronchoalveolar lavage fluid (BALF) levels of inflammatory cells, cytokine, and immunoglobulin were monitored at (3, 7, and 14 days after BDL surgery). Moreover, lung tissue histopathological alterations and biomarkers of oxidative stress were evaluated. Results: A significant increase in BALF inflammatory cells, TNF-α, and immunoglobulin G (IgG) was evident in BDL animals. Moreover, the infiltration of inflammatory cells, vascular congestion, and hemorrhage were detected in the lung of BDL rats. Increased markers of oxidative stress were also evident in the lung of BDL animals. Sildenafil (10 and 20 mg/kg) significantly blunted inflammatory response, oxidative stress, and histopathological alterations in the lung of cholestatic animals. Conclusion: The effects of sildenafil on inflammatory response and oxidative stress biomarkers seems to play a crucial role in its protective properties in the lung of cholestatic animals.

Evaluating the mitochondrial function is probably one of the most investigated fields for detecting the mechanism of drug-induced cytotoxicity and organ injury. Several drugs have been known for their adverse effects on the mitochondria. Drugs could affect the cellular power plants through various mechanisms. The inhibition of electron transport chain, induction of mitochondrial permeabilization, enhancing the dissipation of mitochondrial membrane potential, induction of disintegrity, and disruption of mitochondrial membranes, and the inhibition of a wide range of enzymes involved in the mitochondrial function have been studied as mechanisms of drug-induced mitochondrial impairment. Drug-induced mitochondrial impairment could affect the drug discovery process or cause the withdrawal of drugs from the market. Therefore it is essential to evaluate the adverse effects of drugs on mitochondrial function. This chapter will provide a broad overview of the mechanisms of drug-induced mitochondrial impairment. Moreover, the challenges in assessing xenobiotics-induced mitochondrial injury, testing systems, and biomarkers are highlighted. Finally, the role of protective strategies against drug-induced mitochondrial impairment is discussed. These studies could lead to discovering more safe pharmaceuticals, finding reliable biomarkers of organ injury, and developing therapeutic strategies against drug-induced toxicity.

Ammonium ion (NH4+) is the major suspected molecule responsible for neurological complications of hepatic encephalopathy (HE). No specific pharmacological action for NH4+-induced brain injury exists so far. Excitotoxicity is a well-known phenomenon in the brain of hyperammonemic cases. The hyperactivation of the N-Methyl-d-aspartate (NMDA) receptors by agents such as glutamate, an NH4+ metabolite, could cause excitotoxicity. Excitotoxicity is connected with events such as oxidative stress and neuroinflammation. Hence, utilizing NMDA receptor antagonists could prevent neurological complications of NH4+ neurotoxicity. In the current study, C57BL6/J mice received acetaminophen (APAP; 800 mg/kg, i.p) to induce HE. Hyperammonemic animals were treated with ketamine (0.25, 0.5, and 1 mg/kg, s.c) as an NMDA receptor antagonist. Animals' brain and plasma levels of NH4+ were dramatically high, and animals' locomotor activities were disturbed. Moreover, several markers of oxidative stress were significantly increased in the brain. A significant increase in brain tissue levels of TNF-& alpha;, IL-6, and IL-1 & beta; was also detected in hyperammonemic animals. It was found that ketamine significantly normalized animals' locomotor activity, improved biomarkers of oxidative stress, and decreased proinflammatory cytokines. The effects of ketamine on oxidative stress biomarkers and inflammation seem to play a key role in its neuroprotective mechanisms in the current study.

Understanding the intricate molecular mechanisms governing aryl hydrocarbon receptor (AHR) and Wnt/β-Catenin pathways crosstalk is of paramount importance for elucidating normal development. We investigated the repercussions of aberrant activation of these signaling pathways on kidney development. HEK-293 cells were subjected to AHR and Wnt activators and inhibitors for 3 and 24 h. Subsequently, pregnant adult female BALB/c mice were administered treatments at gestation day 9 (GD-9), and embryos were analyzed at GD-18 using a combination of cellular, molecular, stereological, and histopathological techniques. Our results demonstrated a noteworthy escalation in oxidative stress and gene expression endpoints associated with apoptosis. Moreover, stereological analyses exhibited alterations in cortex, proximal tubule, and kidney tissue vessels volumes. Remarkably, co-treatment with 6-formylindolo [3,2-b] carbazole (FICZ) and cadmium (Cd) resulted in a significant reduction in glomerulus volume, while elevating the volumes of distal tubule, Henle loop, and connective tissue, compared to the control group. Histopathological investigations further confirmed structural changes in the loop of Henle and proximal tubule, alongside a decline in glomerular volume. Additionally, the expression levels of AHR and Ctnnb1 genes significantly increased in the Cd-treated group compared to the control group. Enhanced expression of apoptosis-related genes, including Bcl-x , Bax , and Caspase3 , along with alterations in mitochondrial membrane potential and cytochrome C release, was observed. In contrast, Gsk3 gene expression was significantly decreased. Our findings robustly establish that chemical pollutants, such as Cd, disrupt the AHR and Wnt/β-Catenin physiological roles during developmental stages by inhibiting the metabolic degradation of FICZ.

Background and objectives: Aluminum phosphide (AlP), known as "rice tablet," is widely used as an effective pesticide. However, AlP poisoning is a common cause of mortality in many countries, such as Iran. Unfortunately, there is no specific antidote for AlP toxicity to date. AlP releases phosphine gas when it is exposed to moisture or acid. Phosphine is a potent mitochondrial toxin that could significantly inhibit cellular energy metabolism. AlP poisoning is an emergency con-dition that needs instant and effective intervention. Dihydroxyacetone (DHA) is a simple saccharide used for several pharmacological as well as cosmetic purposes. Previously, we found that DHA could significantly prevent mitochondrial impairment induced by toxic agents such as cyanide and phosphine in various in vitro and in vivo experimental models.Methods: Hospitalized patients (n = 111) were evaluated for eligibility criteria. Among these patients, n = 35 cases were excluded due to incomplete data (n = 11) and suspicion of poisoning with poisons other than AlP (n = 24). Meanwhile, n = 76 cases with confirmed AlP poisoning were included in the study. AlP-poisoned patients who did not receive DHA (n = 18) were used as the control group. Patients (n = 58) received at least one dose of DHA (500 ml of 5 % DHA solution w/v, i.v.) as an adjuvant therapy in addition to the routine treatment of AlP poisoning. Arterial blood gas (ABG), blood pH, bicarbonate levels, and other vital signs and biochemical measurements were monitored. Moreover, the mortality rate and hospitalization time were evaluated in DHA-treated and AlP-poisoned patients without DHA administration. Several biomarkers were assessed before (upon hospitalization) and after DHA treatment. The routine tests for AlP-poisoned patients in this study were the measurement of electrolytes (K+ and Na+), WBC, RBC, hemoglobin, INR, carbonate (HCO3), blood pH, PaCO2, and PaO2 and SGPT, SGOT, BUN, Cr.Results: Upon patients' admission, significant decreases in blood pH (acidosis), blood PaO2, and HCO3 levels were the hallmarks of AlP poisoning. It was found that DHA significantly alleviated biomarkers of AlP poisoning and tremendously enhanced patients' survival rate (65.52 % in DHAtreated vs 33.34 % in the control group) compared to patients treated based on hospital routine AlP poisoning protocols (no DHA). No significant adverse effects were evident in DHA-treated patients in the current study.Interpretation and conclusions: These data suggest that parenteral DHA is a novel and effective antidote against AlP poisoning to be used as an adjuvant in addition to routine supportive treatment.Trial registration: IR.SUMS.REC.1394.102.

Cholestasis is a clinical complication that primarily influences the liver. However, it is well known that many other organs could be affected by cholestasis. Lung tissue is a major organ influenced during cholestasis. Cholestasis-induced lung injury could induce severe complications such as respiratory distress, serious pulmonary infections, and tissue fibrosis. Unfortunately, there is no specific pharmacological intervention against this complication. Several studies revealed that oxidative stress and inflammatory response play a role in cholestasis-induced lung injury. Carnosine (CARN) is a dipeptide found at high concentrations in different tissues of humans. CARN’s antioxidant and antiinflammatory properties are repeatedly mentioned in various experimental models. This study aimed to assess the role of CARN on cholestasis-induced lung injury. Rats underwent bile duct ligation (BDL) to induce cholestasis. Broncho-alveolar lavage fluid (BALF) levels of inflammatory cells, pro-inflammatory cytokines, and immunoglobulin were monitored at scheduled intervals (7, 14, and 28 days after BDL). Moreover, lung tissue histopathological alterations and biomarkers of oxidative stress were evaluated. A significant increase in BALF inflammatory cells, TNF-α, IL-1β, IL-6, and immunoglobulin-G (IgG) was detected in the BALF of BDL rats. Moreover, lung tissue histopathological changes, collagen deposition, increased TGF-β, and elevated levels of oxidative stress biomarkers were evident in cholestatic animals. It was found that CARN (100 and 500 mg/kg, i.p.) significantly alleviated lung oxidative stress biomarkers, inflammatory response, tissue fibrosis, and histopathological alterations. These data indicate the potential protective properties of CARN in the management of cholestasis-induced pulmonary damage. The effects of CARN on inflammatory response and oxidative stress biomarkers seems to play a crucial role in its protective properties in the lung of cholestatic animals.

Background: of the study: Hepatic encephalopathy (HE) is a complication in which brain ammonia (NH4+) levels reach critically high concentrations because of liver failure. HE could lead to a range of neurological complications from locomotor and behavioral disturbances to coma. Several tactics have been established for subsiding blood and brain NH4+. However, there is no precise intervention to mitigate the direct neurological complications of NH4+.Purpose: It has been found that oxidative stress, mitochondrial damage, and neuro-inflammation play a fundamental role in NH4+ neurotoxicity. Piracetam is a drug used clinically in neurological complications such as stroke and head trauma. Piracetam could significantly diminish oxidative stress and improve brain mitochondrial function.Research methods: In the current study, piracetam (100 and 500 mg/kg, oral) was used in a mice model of HE induced by thioacetamide (TA, 800 mg/kg, single dose, i.p).Results: Significant disturbances in animals' locomotor activity, along with increased oxidative stress biomarkers, including reactive oxygen species formation, protein carbonylation, lipid peroxidation, depleted tissue glutathione, and decreased antioxidant capacity, were evident in the brain of TA-treated mice. Meanwhile, mitochondrial permeabilization, mitochondrial depolarization, suppression of dehydrogenases activity, and decreased ATP levels were found in the brain of the TA group. The level of pro-inflammatory cytokines was also significantly high in the brain of HE animals.Conclusion: It was found that piracetam significantly enhanced mice's locomotor activity, blunted oxidative stress biomarkers, decreased inflammatory cytokines, and improved mitochondrial indices in hyperammonemic mice. These data suggest piracetam as a neuroprotective agent which could be repurposed for the management of HE.

INTRODUCTION:Cholestasis is the stoppage of bile flow, leading to the accumulation of potentially cytotoxic bile components in the liver. These cytotoxic molecules affect many organs. Cholestasis-induced lung injury is a severe complication that could lead to tissue fibrosis and respiratory distress. Substantial evidence indicates the role of oxidative stress and inflammatory response in the pathogenesis of cholestasis-associated pulmonary damage. Agmatine (AGM; 1-amino-4-guanidinobutane) is a biogenic amine endogenously synthesized in the human body. This amine provides potent anti-inflammatory and antioxidant properties.METHODS:In the current study, a series (six C57BL/6J male mice/group) of bile duct-ligated (BDL) animals were monitored at scheduled intervals (7, 14, and 28 days after the BDL operation) to ensure inflammatory response in their lung tissue (by analyzing their bronchoalveolar lavage fluid [BALF]). It was found that the level of inflammatory cells, pro-inflammatory cytokines, and IgG in the BALF reached their maximum level on day 28 after the BDL surgery. Therefore, other research groups were selected as follows: 1) Sham-operated (2.5 mL/kg normal saline, i.p., for 28 consecutive days), 2) BDL, 3) BDL + AGM (1 mg/kg/day, i.p., for 28 consecutive days), and 4) BDL + AGM (10 mg/kg/day, i.p., for 28 consecutive days). Then, the BALF was monitored at scheduled time intervals (7, 14, and 28 days post-BDL).RESULTS:It was found that pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), bile acids, bilirubin, and inflammatory cells (monocytes, neutrophils, and lymphocytes) were significantly increased in the BALF of BDL mice. Moreover, biomarkers of oxidative stress were significantly increased in the pulmonary tissue of cholestatic animals. Lung tissue histopathological changes, tissue collagen deposition, and increased TGF-β were also detected. It was found that AGM significantly ameliorated cholestasis-induced lung injury.CONCLUSION:The effects of AGM on inflammatory indicators, oxidative stress biomarkers, and tissue fibrosis seem to play a pivotal role in its protective properties.

Aim of the study:Cholestasis/cirrhosis could induce erythrocyte lysis. The incidence of various types of anemia in cirrhosis is approx. 75%. Several studies have mentioned the pivotal role of oxidative stress in this complication. Taurine (TAU) is the human body's most abundant free amino acid. TAU is known as a robust cell membrane stabilizer. Many studies have mentioned that TAU could counteract oxidative stress in various experimental models. The current study was intended to evaluate the effect of TAU on erythrocytes in cirrhotic rats.Material and methods:Bile duct ligation (BDL) surgery was carried out on rats. Then, complete blood count (CBC), hemoglobin (Hgb), hematocrit (HTC), and erythrocytes' G6PD, catalase (CAT), and superoxide dismutase (SOD) activity were measured. Moreover, biomarkers of oxidative stress were assessed, and the erythrocytes' morphological changes were monitored in the cirrhotic mice exposed to TAU (0.25%, 0.5%, and 1% w : v in drinking water).Results:Significant changes in the assessed erythrocyte parameters (G6PD activity, Hgb, HTC, and erythrocyte count) and red blood cells (RBC) morphological alterations were detected on day 42 after BDL surgery. Biomarkers of oxidative stress also did not change at the time points, except on post-BDL days 28 and 42. A significant decrease in blood parameters was evident at post-BDL day 42. All doses of TAU (0.25%, 0.5%, and 1% w : v in drinking water) significantly improved erythrocyte parameters and encountered oxidative stress in the erythrocytes of cirrhotic animals.Conclusions:These data indicate that TAU could be a safe agent to mitigate cirrhosis-induced erythrocyte damage and anemia. Further investigations are necessary to prove this in clinical settings.