This study investigated the protective effects of taurine against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced cardiotoxic damage in rats. Adult male Wistar rats (250-300 g) were randomly assigned to four groups (n = 8 per group): Control, TCDD, TAU, and TCDD + TAU. TCDD (2 μg/kg/week) and/or taurine (200 mg/kg/day) were administered via gavage for 30 days. Following the experimental period, heart tissue samples were collected for analysis. Oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD) activity, and glutathione (GSH) levels, were assessed using biochemical methods. Histopathological and immunohistochemical evaluations of cardiac tissue were also performed. The TCDD group showed significantly increased TBARS levels (p < 0.05) and decreased SOD activity and GSH levels (p < 0.001) compared with the Control group. In contrast, taurine co-administration significantly increased SOD activity and GSH levels while reducing TBARS levels relative to the TCDD group. Moreover, TCDD exposure induced marked histopathological alterations in heart tissue, whereas taurine co-administration attenuated these structural alterations. Immunohistochemical findings indicated that taurine attenuated TCDD-induced apoptosis by reducing caspase-3 activation. Overall, taurine effectively mitigated TCDD-induced oxidative stress, histopathological damage, and apoptotic signaling in cardiac tissue, suggesting that taurine co-administration may exert protective effects against TCDD-induced cardiotoxicity.

Objective criteria are essential in forensic toxicology for elucidating combustion-related deaths. Carbon monoxide (CO) and carbon dioxide (CO₂) impair oxygen delivery by competing with oxygen for hemoglobin binding and by disrupting cellular oxidative metabolism. This study aimed to evaluate biochemical changes in blood and brain tissues, neuroglobin gene expression in the brain, and histopathological alterations following CO and CO₂ exposure in rats, hypothesizing differential neuroglobin responses between the two gases. Twenty-four male Wistar albino rats (300 ± 50 g) were randomly divided into three groups and exposed to either carbon monoxide (0.05%), carbon dioxide (20%), or no gas (control) in a controlled glass isolation chamber. Blood and brain samples were collected for toxicological, genetic, and histopathological analyses. Blood gas analyses revealed intergroup differences in pH and bicarbonate levels, indicating altered oxidative balance. Antioxidant enzyme activity suggested increased oxidative stress in both exposure groups. Histopathological examination demonstrated more severe neuronal damage in the carbon monoxide-exposed group compared with the carbon dioxide and control groups. Neuroglobin expression levels showed intergroup variation but did not reach statistical significance. Both CO and CO₂ exposure induced oxidative stress-related changes, with carbon monoxide causing more pronounced neuronal injury. Although neuroglobin levels tended to increase following exposure, the differences were not statistically significant. Further experimental studies may enhance understanding of neuroglobin's role in forensic toxicology. [Med-Science 2026; 15(2.000): 985-94]

Letrozole, a widely used aromatase inhibitor for hormone receptor-positive breast cancer, has been suggested to be associated with potential neurotoxic effects; however, the underlying mechanisms remain unclear. This study aimed to investigate the neurotoxic effects of letrozole and evaluate the neuroprotective potential of hesperidin, a natural flavonoid with antioxidant and anti-inflammatory properties. Adult female rats received letrozole alone or in combination with hesperidin for 4 weeks. Biochemical analyses showed that letrozole significantly increased total oxidant status (TOS) and decreased total antioxidant status (TAS), indicating oxidative stress. Gene expression results revealed upregulation of pro-apoptotic Bax and downregulation of anti-apoptotic Bcl2 in letrozole-treated rats, reflecting apoptotic activation. Additionally, inflammatory cytokine measurements demonstrated elevated pro-inflammatory markers (IL-1, IL-6, TNF-α) and reduced anti-inflammatory IL-10 following letrozole administration. Histopathological examination revealed cortical microhemorrhages, edema, and hyperemia. Importantly, co-treatment with hesperidin attenuated oxidative imbalance, normalized apoptotic gene expression, modulated inflammatory cytokine levels towards an anti-inflammatory profile, and ameliorated histological damage. These findings indicate that hesperidin confers neuroprotection by restoring redox balance, regulating apoptosis, and suppressing inflammation in letrozole-induced neurotoxicity. Further studies are warranted to elucidate the precise molecular mechanisms and potential therapeutic applications of hesperidin in letrozole-induced neurotoxicity.

Mancozeb (MNZ), a widely used dithiocarbamate fungicide, has been associated with oxidative stress-mediated organ toxicity in nontarget species. The present study investigated the potential protective effects of N-acetylcysteine (NAC) against MNZ-induced hepatotoxicity and nephrotoxicity in rats. Thirty-two adult male Wistar rats were randomly assigned to four groups: Control, NAC (200 mg/kg, i.p.), MNZ (500 mg/kg, p.o.), and MNZ + NAC for 28 days. Serum biochemical parameters, tissue oxidative status, inflammatory cytokine levels, apoptosis-related gene expression, and histopathological alterations were evaluated in liver and kidney tissues. MNZ administration significantly elevated serum ALT, AST, GGT, bilirubin, creatinine, and urea levels compared with controls (p < 0.05). In both liver and kidney tissues, MNZ caused a significant increase in the oxidative stress index (OSI) by elevating total oxidant status (TOS) and reducing total antioxidant status (TAS) (p < 0.001). Pro-inflammatory cytokines (IL-1β, IL-6) and the mRNA expression of TNF-α, iNOS, COX-2, Bax, and caspase-3 were significantly upregulated, whereas Bcl-2 expression and the Bcl-2/Bax ratio were reduced. Histopathological evaluation confirmed substantial structural deterioration in both organs. NAC co-administration significantly attenuated biochemical abnormalities, restored redox balance, modulated inflammatory and apoptotic gene expression, and markedly improved tissue architecture. These findings indicate that MNZ induces hepatorenal injury through oxidative stress-associated inflammatory and apoptotic processes, and that NAC confers significant protective effects by restoring cellular redox homeostasis and limiting downstream tissue damage.

This study aimed to investigate whether 18β-glycyrrhetinic acid (GA) could protect against cadmium-induced testicular damage in male rats. Twenty-four adult male Sprague Dawley rats were randomly divided into four groups (n = 6): Control, Cadmium (CAD), GA, and Cadmium + GA. Cadmium and GA were administered at doses of 1 mg/kg and 100 mg/kg, respectively, for 50 days. At the end of the experimental period, testicular and epididymal tissues were collected for biochemical, molecular, histopathological, and immunohistochemical analyses. Biochemical evaluations included oxidative stress parameters (TAS, TOS) and inflammatory cytokines (TNF-α, IL-6). Apoptotic gene expression (Bcl-2, Bax, Caspase-3) was assessed by RT-PCR. Histopathological and immunohistochemical analyses were performed to evaluate Bcl-2, Bax, iNOS, and NF-κB expression. Cadmium exposure significantly increased oxidative stress and inflammatory cytokine levels and induced marked histological damage, including Leydig cell necrosis and severe tubular degeneration. Immunohistochemical analysis revealed increased Bax, iNOS, and NF-κB expression in testicular and epididymal tissues. Cadmium also upregulated Bax and Caspase-3 while downregulating Bcl-2 gene expression. Conversely, GA treatment significantly attenuated cadmium-induced oxidative stress, inflammation, apoptosis, and histological damage. These findings suggest that GA exerts protective effects against cadmium-induced testicular toxicity and may represent a promising therapeutic agent for preventing cadmium-related male infertility.

Di-n-butyl phthalate (DBP), a widely used plasticizer, induces oxidative stress and neurotoxicity through the generation of reactive oxygen species. Ellagic acid (EA), a natural polyphenolic antioxidant, may counteract these effects. This study aimed to evaluate the protective role of EA against DBP-induced oxidative brain injury. Thirty-two male rats were randomly divided into four groups: Control, DBP, EA, and DBP+EA. DBP was administered orally at a dose of 500 mg/kg/day, while EA was given by gavage at 2 mg/kg/day for four weeks. Oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities were analyzed in brain tissue. DBP exposure significantly increased TBARS levels while decreasing GSH and SOD activities, indicating lipid peroxidation and antioxidant depletion. In contrast, CAT activity was elevated, suggesting a compensatory enzymatic response to excess hydrogen peroxide. EA treatment markedly attenuated oxidative damage by restoring GSH and SOD levels and normalizing CAT activity. These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.

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: 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-1 beta, IL-6, estradiol, and FSH levels (p<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-alpha gene expression. HSP and TAU did not significantly alter hormone levels (p>0.05). However, HSP significantly reduced oxidative stress (p<0.05), decreased the expression of genes related to apoptosis and inflammation (p<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-1 beta and IL-6 levels or the expression of apoptosis-related genes (p>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.

Beta-glucans (βTGs) are a class of dietary fibers and biologically active polysaccharides derived from natural sources, known for their diverse bioactive properties. Their documented effects include anti-tumor, anti-inflammatory, prebiotic, anti-obesity, anti-allergic, anti-microbial, antiviral, anti-osteoporotic, and immunomodulating activities. Despite these well-established benefits, the role of βTG in dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome (PCOS) remains largely unexplored. This study investigated the protective effects of βTG treatment on PCOS and its potential to reverse PCOS-induced changes. Female Sprague-Dawley (SD) rats were randomly divided into four groups (n = 8 each): control, PCOS, PCOS+βTG, and βTG. We assessed biochemical markers related to oxidative stress, antioxidant status, inflammation, cytokines, and hormone levels. Additional analyses included immunohistochemistry and histopathology. Membrane array analysis was used to profile growth factors, cytokines, and chemokines. However, βTG normalized deviations in the estrous cycle caused by PCOS and positively affected the reproductive system (p < 0.05). It also reduced the inflammatory response in PCOS rats by decreasing inflammatory cytokines (p < 0.05). Furthermore, oxidative stress was significantly reduced, and antioxidant enzyme activities were markedly elevated in the βTG group (p < 0.05). Histopathological alterations were prevented by βTG, which also induced the expression of essential proteins such as beta-nerve growth factor (bNGF), tissue inhibitor of metalloproteinase-1 (TIMP-1), Agrin, cytokine-induced neutrophil chemoattractant-1 (CINC-1), brain-derived neurotrophic factor (BDNF), and basic fibroblast growth factor (FGF-2/bFGF) (p < 0.05). In conclusion, βTG treatment effectively protects against oxidative stress, inflammation, hormone imbalance, and histopathological damage in ovarian tissue caused by PCOS.

Purpose: This study aimed to investigate the protective effects of insulin-like growth factor-1 (IGF-1) against doxorubicin (DOX)-induced liver and kidney damage in rats using biochemical, immunohistochemical, and histopathological methods. Materials and Methods: A total of 32 Wistar albino rats were randomly assigned into four groups: Control, DOX (4 mg/kg/week), IGF-1 (1 µg/kg daily), and DOX + IGF-1 (DOX 4 mg/kg/week + IGF-1 1 µg/kg daily). After the four-week experimental protocol, blood, liver, and kidney tissues were collected under anesthesia. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), urea, and creatinine were analyzed biochemically. Total antioxidant status (TAS) and total oxidant status (TOS) in liver and kidney tissues were measured using ELISA. Gene expression levels of HIF-1α and iNOS were evaluated by real-time PCR. Histopathological and immunohistochemical (Caspase-3, TNF-α, and FGF-2) evaluations were conducted on liver and kidney tissues. Results: DOX significantly increased serum ALT, AST, BUN, urea, and creatinine levels and elevated TOS while reducing TAS in tissues). HIF-1α expression was markedly upregulated (+5.50-fold), indicating oxidative damage. IGF-1 administration reduced serum ALT, AST, BUN, urea, and creatinine levels, increased TAS, and decreased TOS. Expression levels of HIF-1α and iNOS approached those of the control group. DOX caused significant histopathological damage and increased Caspase-3 and TNF-α expressions in the liver and Caspase-3 and FGF-2 expressions in the kidney. These alterations were ameliorated by IGF-1 treatment. Conclusion: The findings suggest that IGF-1 exerts protective effects against DOX-induced hepatorenal toxicity, possibly through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

This study aimed to demonstrate the protective effect of 1,8-cineole against Aroclor 1254 (A1254)-induced liver toxicity in male rats and to elucidate the underlying mechanisms. A1254 is among the persistent organic pollutants and is a toxic substance that can cause serious damage to various organs such as the liver, brain, and lungs. 1,8-cineole, a monoterpene, possesses significant pharmacological activities such as antioxidant, anti-inflammatory, and anticancer effects. Thirty-two healthy young (4-6 weeks) male Wistar albino rats (200-300 g) were used. The animals were randomly divided into four equal groups: Control, Aroclor, Cineole, and Aroclor+Cineole (n = 8). Rats were daily administered A1254 (1 mg/kg, intraperitoneally) either alone or in combination with 1,8-cineole (100 mg/kg orally in corn oil) for 30 days. The liver tissues and serum were collected from the rats under anesthesia. The protective effect of 1,8-cineole against A1254-induced liver damage was demonstrated using ELISA, RT-PCR, histopathological analysis, and immunohistochemical evaluation methods. A1254 administration increased the total oxidant status (TOS) level and triggered oxidative stress by decreasing the total antioxidant status (TAS). However, 1,8-cineole significantly reduced TOS levels and increased TAS levels in serum and liver tissues (p < 0.05). A1254 increased the pro-apoptotic Bax gene expression in liver tissues, while 1,8-cineole significantly decreased (p < 0.05). Similarly, A1254 increased the gene expressions of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1-beta (IL-1β), inducible nitric oxide synthase (iNOS), and interferon-gamma (INF-γ) in liver tissues, whereas 1,8-cineole decreased the expression of these genes (p < 0.05). Moreover, 1,8-cineole reduced the histopathological changes associated with A1254-induced oxidative stress and inflammation in liver tissues. In conclusion, 1,8-cineole may be a protective agent due to its anti-apoptotic effect, reduction of oxidative damage, anti-inflammatory efficacy, and amelioration of histopathological changes in liver toxicity.

Docetaxel (Dtx) is a frequently used antineoplastic agent despite its dose-limiting toxic effects. Our objective was to assess the effects of oleuropein (Ole), a natural polyphenol, on Dtx-induced toxicity. Thirty-two male rats were randomly assigned to four groups for a four-week treatment: Control (sham), Dtx (5 mg/kg weekly, i.p.), Ole (30 mg/kg daily, p.o.) and Dtx+Ole. Biochemical and gene expression analyses were performed on liver, kidney and blood samples. Additionally, histological and immunohistochemical evaluations were conducted on the liver and kidneys. Ole reduced the Dtx-induced oxidative stress index in tissues. In contrast to Dtx, it decreased caspase-3 and Bax gene expressions while increasing Bcl-2 expression. Furthermore, Ole improved the ALT, AST, urea and creatinine levels, which were impaired by Dtx administration. It also reduced serum IL-6, IL-1β and TNF-α levels, which had been elevated due to Dtx. Histopathological and immunohistochemical examinations revealed that Ole administration mitigated Dtx-related damage in both tissues. These findings suggest that Ole might offer protection against Dtx-induced liver and kidney toxicity in rats.

Nivolumab is an effective immunotherapy drug, but its long-term side effects remain unknown. This study was designed as a preventive experimental model to investigate the potential preventive and protective effects of hesperidin against testicular toxicity that may be caused by nivolumab. Thirty-two male Wistar Albino rats were used in the study (n = 8 per group). The groups were as follows: control, nivolumab (3 mg/kg), hesperidin (50 mg/kg), and nivolumab (3 mg/kg) + hesperidin (50 mg/kg). After the completion of drug administration, blood and testicular tissues were collected under anesthesia. ELISA, real-time PCR, and histopathological analyses were performed to assess the biochemical, molecular, and histopathological changes in the testicular tissue. Histopathological analysis revealed that nivolumab caused notable damage to the testicular tissue. Severe cytoplasmic expression of 8-hydroxyguanosine (8-OHdG) and Caspase-3 was observed in spermatocytes, indicating oxidative stress and apoptosis. Hesperidin administration attenuated these histopathological changes. Biochemical analysis showed that nivolumab disrupted the balance of total oxidants and antioxidants, leading to oxidative stress, whereas hesperidin enhanced antioxidant activity and reduced oxidative damage. Additionally, nivolumab significantly reduced serum testosterone levels, while hesperidin increased testosterone levels. In terms of molecular pathways, nivolumab downregulated PI3K, AKT, and MTOR expressions, disrupting this signaling cascade, while hesperidin restored these expressions to levels closer to the control group. Nivolumab also reduced PD-1 expression, but hesperidin did not alter PD-1 expression levels. This preventive experimental design demonstrated that nivolumab caused oxidative damage and histopathological changes in rat testicular tissue, whereas hesperidin provided preventive protection against these adverse effects through its antioxidant and anti-apoptotic properties.

Bleomycin (BLM), a chemotherapeutic agent commonly used in cancer treatment, is associated with oxidative stress and testicular toxicity, leading to impaired reproductive health. Hesperidin (HES), a citrus-derived flavonoid with strong antioxidant properties, has the potential to counteract these adverse effects. This study aimed to evaluate the protective effects of HES against the reproductive toxicity induced by BLM, focusing on oxidative stress, sperm characteristics and histological changes in the male reproductive system. Thirty-two rats were divided into four groups: Control, BLM, HES and BLM + HES. BLM was administered intraperitoneally at 10 mg/kg twice a week, while HES was given orally at 50 mg/kg/day for 30 days. The findings revealed that BLM induced significant oxidative stress by promoting lipid peroxidation and impairing antioxidant defence mechanisms in the testis. Additionally, BLM treatment caused a marked decline in sperm motility, an increase in abnormal sperm rates and severe histopathological damage in testicular tissue. However, co-administration of HES significantly mitigated these adverse effects by improving oxidative balance, restoring sperm quality and reducing histopathological injuries. In conclusion, HES demonstrated potential in alleviating BLM-induced reproductive toxicity, suggesting its therapeutic role in protecting against chemotherapy-induced male infertility.

Paclitaxel (PAC), derived from Taxus brevifolia, is used to treat solid tumours but causes reproductive toxicity due to oxidative stress, affecting sperm quality and testicular tissue. Nerolidol (NRL), an antioxidant sesquiterpene alcohol, has not been studied for its potential to reduce PAC-induced reproductive damage. This study investigates NRL's ability to mitigate PAC-induced reproductive toxicity in rats. Forty healthy adult male Spraque Dawley rats were randomly divided into four equal groups (Control, PAC, NRL, PAC + NRL). PAC was given intraperitoneally at a dose of 2 mg/kg once a week for 4 weeks. NRL was given orally at a dose of 100 mg/kg/day for 4 weeks. Control group received PAC and NRL vehicles. After 4 weeks, testis tissue samples were collected, and parameters, including oxidants, antioxidants, sperm motility, density, abnormal spermatozoon ratios and cytokines, were measured. PAC administration increased oxidant levels and decreased antioxidant enzyme activities. Nerolidol mitigated these alterations significantly. Similarly, PAC elevated IL-1, IL-6, TNF-α levels and lowered IL-10 levels, these effects attenuated by nerolidol in the PAC + NRL group. In conclusion, it was determined that PAC induces reproductive toxicity through oxidative stress, and NRL demonstrates potential in ameliorating these effects through its antioxidant activity.

We investigated the effects of beta-glucan (beta g) on kidney and liver damage caused by cisplatin (CP), an antineoplastic agent widely used to treat many types of cancer, in a rat model. The side effects of CP in many tissues and organs limit its usage. beta g is a natural polysaccharide that is an effective free radical scavenger. A total of 28 rats were randomly divided into four groups. Group 1 was a non-intervention control, only feed and water were given. Group 2 was administered 7 mg/kg CP in a single dose. Group 3 was administered 50 mg/kg beta g orally for 14 days. Group 4 was administered beta g for 14 days, following a single dose of CP. At the end of the experiment, kidney and liver tissues were evaluated biochemically and histopathologically. Increased thiobarbituric acid-reactive substances (TBARS) levels, as well as decreased catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) levels, as well as histological damage, were noted in both the kidney and liver tissues of the CP group. However, beta g treatment prevented the oxidative and histopathological effects of CP. The study demonstrates the protective efficacy of beta g against CP-induced kidney and liver damage through the effect of its antioxidant properties.

Grapevine Roditis leaf discoloration-associated virus (GRLDaV) is a type of virus that infects grapevines. This research aimed to determine the prevalence of GRLDaV in Turkey vineyards and investigate the genetic diversity and population structure of the selected viral isolates from Turkey compared to isolates from other countries. In this study, 800 shoot samples from Turkey vineyards were collected in late spring and autumn from different regions. The samples were analysed by RT-PCR targeting the partial RNaseH-like gene region of the virus genome. The overall prevalence of GRLDaV was 8.1% among the samples. Phylogenetic analysis of the GRLDaV genome showed that the GRLDaV isolates were clustered into two major lineages. The nucleotide diversity (pi) value of Group I, including only Mediterranean isolates, was lower than Group II, suggesting little variation among isolates. Even though pi values were low among the geographical regions in Turkey, the region with the highest nucleotide diversity was the Aegean population, followed by the Eastern and Mediterranean populations. Comparison between nonsynonymous and synonymous substitutions showed that negative selection acts on synonymous amino acids. Along with neutrality tests and gene flow analyses, it was emphasized that genetic drift played an important role in shaping the GRLDaV populations. This study provides important information on the prevalence and genetic diversity of GRLDaV in Turkey vineyards. The findings will help to develop better strategies to manage and control this virus, which can cause significant economic losses in grape industries.

Abstract Objective Sleep health, mental health and cardiovascular health are multidimensional constructs that are strongly associated with each other. Anxiety and depression are the most common psychiatric diseases in the community and frequently comorbid in routine clinical practice. This study sought to investigate whether there is an association between sleep quality and echocardiographic parameters in patients with anxiety and/or depression. Methods The clinical and instrumental find­ings of consecutive patients diagnosed with either of anxiety disorders and/or depressive disorders and underwent cardiac examination in our tertiary center on the same day were retrospectively reviewed. The diagnosis was made by a psychiatrist according to the criteria listed in the fifth edition of The Diagnostic and Statistical Manual of Mental Disorders. Afterwards, Hospital Anxiety and Depression Scale (HADS) and Pittsburgh Sleep Quality Index (PSQI) were applied to patients to assess symptom severity and sleep quality, respectively. Subsequent to psychiatric examination, the patients underwent echocardiographic examination that includes two-dimensional conventional echocardiography, tissue doppler imaging (TDI) echocardiography, atrial conduction times, and left atrium (LA) volumes and functions. Results The final study population consisted of 167 patients and divided into two groups according to their PSQI score: PSQI<5 (normal sleep quality) (n=32) and PSQI≥5 (impaired sleep quality) (n=135). Aortic diameter, left ventricular (LV) end-systolic diameter, LV end-diastolic and -systolic volume, LV stroke volume and LV stroke volume index, LV outflow tract velocity–time integral (LVOT-VTI), and LA conduit volume calculations were significantly lower in patients with impaired sleep quality compared to patients with normal sleep quality. The other echocardiographic parameters including LV systolic functions, doppler and TDI echocardiography indices, atrial conduction times, atrial mechanical functions including LA function index (LAFI) were similar among groups. Correlation analysis yielded a negative, weak but statistically significant correlation between LAFI and PSQI score (r=-0.17, p=.030) (Figure 1A). Left intra-AEMD positively and significantly correlated with PSQI score at a weak level (r=0.16, p=.043) (Figure 1B). Aortic diameter, LV stroke volume index, LVOT-VTI and conduit volume were determined as echocardiographic parameters significantly associated with impaired sleep quality in univariate analysis. Among these parameters, only conduit volume remained as significant and independent associate of impaired sleep quality in multivariate logistic regression analysis (Odds ratio:0.91, 95% Confidence interval:0.85-0.98, p=.018) (Table 1). Conclusion There is an independent association between LA conduit volume and impaired sleep quality in patients suffering from anxiety and/or depressive disorders.Figure 1Table 1

Favipiravir is a nucleoside analogue antiviral drug and inhibits the replication of many RNA viruses, especially influenza viruses. Favipiravir has also been used to treat patients with mild to moderate COVID-19 disease. However, various side effects, including neurological side effects, have been reported related to the use of favipiravir. Therefore, in this study, we aimed to investigate the possible effects of favipiravir alone or in combination with vitamin C on aged rats' brain tissue and the possible mechanisms of these effects. A total of 30 rats used in the study were randomly divided into 5 equal groups and the first group was kept as the control group. High-dose (100 mg/kg) or low-dose (20 mg/kg) favipiravir was administered alone or in combination with vitamin C (150 mg/kg) to other groups. Administration of both high and low doses of favipiravir significantly increased TBARS levels in brain tissue of aged rats. Similarly, both high and low doses of favipiravir led to significant increases in Bcl-2 and caspase-3 relative mRNA expression. However, only low dose favipiravir caused a significant increase in iNOS and IL-1β relative mRNA expression levels. Similar results were also observed in histopathological examinations. However, co-administration of vitamin C with favipiravir attenuated some of the adverse effects of favipiravir. In conclusion, in this study, it was shown that the use of favipiravir caused some adverse effects through oxidative, inflammatory and apoptotic processes in the brain tissue of aged rats, and the potential of vitamin C to alleviate these effects.

Doksorubisin, çeşitli katı tümörlerin tedavisinde yaygın olarak kullanılmaktadır. Doksorubisin güçlü antineoplastik aktivitesine rağmen kardiyotoksik etkisi nedeniyle kullanımı sınırlıdır. Bu çalışmada doksorobusin kaynaklı kardiyotoksisitede insülin benzeri büyüme faktörünü (IGF)-1 koruyucu rolünü değerlendirilmesi amaçlandı. Otuz iki adet sıçan 4 gruba ayrıldı: Kontrol, Doksorubisin (4 mg/kg/hafta), IGF-1 (2 günde bir 1 µg /kg), doksorubisin (4 mg/kg/hafta)+ IGF-1 (2 günde bir 1 µg /kg).Doksorubisin ve IGF-1 intraperitoneal olarak uygulandı. Dört hafta süren ilaç uygulamalarının ardında anestezi altında kalp ve kan örnekleri alındı. Biyokimyasal analizlerde kan serumundan CK-MB ve Troponin-I seviyeleri ölçüldü. Kalp dokusunda TAS, TOS, TNF-α, ve IL-6 düzeyleri ELISA yöntemiyle ölçüldü. iNOS, HIF-1α, SERCA2a, LC3, Beclin-1 ve SQSTM1 mRNA ekpresyon düzeyleri RT-PCR ile analiz edildi. Histolojik ve immünohistokimyasal (Kaspaz-3 ve ICAM-1) analizler yapıldı. Doksorubisin kalp hızını azaltırken kuyruk kan basıncını düşürdü ve serum CK-MB ve Troponin-I seviyelerini artırdı. Doksorubisin kalp dokusunda total antioksidan/oksidan dengeyi oksidan lehine çevirdi ve TNF-α ve IL-6 sitokin seviyelerinde artışa neden oldu. Doksorobusin kalp dokusunda HIF-1α, SERCA2a, LC3, Beclin-1 ve SQSTM1 mRNA ekpresyon düzeylerini artırdı. Sıçan kalp dokusunda histolojik hasara ve şiddetli Kaspaz-3 ve ICAM-1 ekpresyonlarına neden oldu. IGF-1’ ile birlikte uygulanması doksorubisin toksik etkilerini azalttı. IGF-1’in antioksidan, antiinflamatuar ve antiapoptotik etkilerle doksorubisin kaynaklı kardiyotoksisiteyi iyileştirebileceğini sonucuna ulaşıldı.