Acetaminophen is widely used among humans as an antipyretic and analgesic. In this study, the protective effect of losartan in hepatotoxicity and nephrotoxicity induced by acetaminophen in mice was investigated owing to its anti-inflammatory and antioxidant effects. An injection of a single dose of 500 mg/kg (i.p.) acetaminophen was administered to induce hepatotoxicity and nephrotoxicity in Groups VI–X. Losartan at doses of 1 mg/kg (Group VII), 3 mg/kg (Group VIII), and 10 mg/kg (Groups III, V, IX, and X) was injected intraperitoneally twice, at 1 and 12 h after the acetaminophen injection. Additionally, a 4 mg/kg dose of GW9662 (peroxisome proliferator-activated receptor gamma (PPAR-γ) antagonist) was injected intraperitoneally 30 min before the losartan injections in Groups V and X. At the end of 24 h, the mice were euthanized, and blood, liver, and kidney tissue samples were collected. Levels of AST, ALT, creatinine, and oxidative stress markers including TBARS, SOD, CAT, GPx, TAS, TOS, GSH, and GSSG, along with pro-inflammatory cytokines IL-1β, IL-6, IL-8, IL-10, IL-17, and TNF-α, were measured using ELISA kits. Additionally, a histological evaluation of the tissue samples was performed. Acetaminophen causes increases in the levels of AST, ALT, creatinine, TBARS, TOS, GSSG, IL-1β, IL-6, IL-8, IL-10, IL-17, and TNF-α in serum, liver, and kidney tissue. Meanwhile, it led to a decrease in the levels of SOD, CAT, GPx, TAS, and GSH. Losartan injection reversed oxidative and inflammatory damage induced by acetaminophen. Histopathological changes in liver and kidney tissue were alleviated by losartan. The substance GW9662 increased the protective effect of losartan. In light of all the data obtained from our study, it can be said that losartan has a protective effect on liver and kidney damage induced by acetaminophen due to its antioxidant and anti-inflammatory effects. In terms of the study, losartan was found to be an alternative substance that could protect people from the harmful effects of acetaminophen.

Current chelation treatments used for cadmium poisoning may cause some serious side effects. Thus, safer novel treatments could be promising for clinical use. This study evaluated the effects of cannabidiol on Cd toxicity. Four groups of 10 mice were formed: Groups I and III were cadmium‐free, while groups II and IV received 50 mg/L cadmium in drinking water. Groups III and IV received daily cannabidiol (25 mg/kg) via intragastric gavage. After 30 days, the animals were killed, and blood and tissue samples were collected. Oxidative stress and inflammation markers, including glutathione, catalase, myeloperoxidase, TNF‐α, IL‐1β and IL‐6, were analysed using ELISA. Additionally, histological evaluations of the liver, kidney and testis were performed. Cadmium exposure reduced glutathione and catalase levels in the blood, liver, kidney and testis, while increasing myeloperoxidase. Cannabidiol mitigated these effects on oxidative stress markers. Cannabidiol also reduced the increase in proinflammatory cytokines. Histopathological analysis revealed reduced liver and kidney damage in cannabidiol‐treated groups compared to cadmium‐only groups. In addition, histopathological evaluation showed CBD had no protective effect on the testicular tissue against Cd toxicity. Our results indicate that cannabidiol protects against some toxic effects of cadmium. If confirmed by future studies, cannabidiol may be proposed as a novel treatment for cadmium toxicity.

Amaç Dünya Sağlık Örgütü Akılcı İlaç Kullanımı’nı, “hastaların klinik ihtiyaçlarına uygun ilaçları, kişisel gereksinimlerini karşılayan dozlarda, yeterli bir süre boyunca, kendilerine ve topluma en az maliyet ile kullanmaları” olarak tanımlamıştır. akılcı ilaç kullanımında hastanın, hekimin ve eczacının verdiği talimatlar doğrultusunda ilacını kullanması gerekmektedir. Bu çalışmada Yozgat Bozok Üniversitesi Tıp Fakültesi öğrencilerinin akılcı ilaç kullanımına ilişkin düşüncelerinin değerlendirilmesi amaçlanmıştır. Bulgular Öğrencilerin yaş ortalaması 20,2 ± 1,2, % 47,3’ü erkekti. Öğrencilerin yaklaşık üçte ikisi akılcı ilaç kullanımını hastaya uygun ilaç yazılması olarak tanımladı, öğrencilerin yaklaşık yarısıda akılcı ilaç kullanımı eğitimi aldıklarını ifade etti. Hekimlerce en sık ağrı kesici ilaçların yazıldığını, akılcı ilaç kullanımına en büyük engelin yanlış tanı ve yoğunluktan hasta ile yeterince ilgilenememe olduğu belirtildi. Öğrenciler, Akılcı ilaç kullanımında en önemli paydaşın hekimler olduğunu ve ayrıca aktarlar, televizyon, internet vb. yollarla bitkisel ürünlerin alınarak kullanılmasının, hastaya uygulanacak tedavi sürecinin başarısında olumsuz etkisinin olduğunu ifade etti. Sonuç Akılcı ilaç kullanımına engel olarak görülen hasta muayene süreleri için sağlık yöneticileri tarafından hekimlerin hastası için ayırdığı muayene süresini yeterli düzeye getirecek tedbirlerin (hekim başına düşen hasta sayısı gibi) alınmasının da, akılcı ilaç kullanımı konusunda ilerleme ve katkı sağlayacağını düşündürmektedir.

Aims: Understanding the factors in the etiology of vascular diseases is crucial for prevention. This study assesses the relationship between toxic metal exposure and vascular disease development. Methods: Blood samples from 41 healthy volunteers and 48 cardiovascular disease patients were analyzed using inductively coupled plasma mass spectrometry (ICP-MS). The participants' health data were obtained from hospital records. Results: ICP-MS results showed higher levels of As (5.97 µg/L), Cd (0.44 µg/L), Hg (0.48 µg/L), Pb (37.10 µg/L), Se (75.76 µg/L), Cu (1611.99 µg/L), Mn (14.55 µg/L), Co (0.14 µg/L), Mo (1.93 µg/L), and Ni (0.25 µg/L) in the experimental group. Conversely, Zn (557.0 µg/L), Cr (4.12 µg/L), and Sb (2.35 µg/L) levels were lower. Triglyceride (135.99 mg/dl), folate (8.77 ng/dl), and T3 (1.30 ng/dl) were higher, while HDL (44.13 mg/dl) was lower in the experimental group. Conclusion: These findings suggest a potential relationship between higher exposure to certain toxic metals and the development of vascular diseases. The higher concentrations of toxic metals in the blood of patients with vascular diseases underline the need for further research to confirm these associations and explore potential mechanisms.

Arsenic (As) exposure is known to have harmful effects, prompting the search for effective countermeasures. This study investigated the protective effects of cannabidiol (CBD) against arsenic toxicity in liver cell cultures (THLE-2). The IC50 values for As were determined, finding 10 µM in 2D and 15 µM in 3D cell lines. To assess CBD's protective efficacy, 5 µM of CBD was administered alongside arsenic at its IC50 concentration. The levels of oxidative stress markers, including Glutathione (GSH), malondialdehyde (MDA), myeloperoxidase (MPO), and catalase (CAT), as well as inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), were measured using ELISA kits. Inductively Coupled Plasma Mass Spectrometry (ICP-MS) analysis was conducted to evaluate As uptake in the cells. The results showed that CBD significantly enhanced cell proliferation and reversed the oxidative stress and inflammatory responses induced by arsenic exposure. Furthermore, CBD effectively reduced arsenic uptake into the cells. These findings provide compelling evidence for CBD's protective role against arsenic-induced toxicity, highlighting its potential as a therapeutic agent in mitigating the harmful effects of arsenic