Unusual Excessive Swelling of the Tongue after Calcium Acetate Ingestion: A Case Report

Common side effects of calcium acetate include increased blood calcium levels, nausea-vomiting, diarrhea, and fatigue, while side effects of unknown incidence include \"swelling\". We present the case of an allergic reaction limited to tongue swelling alone, not showing other anaphylactic symptoms. Our case was a female patient who applied to the emergency department with the complaint of isolated tongue swelling three hours after using calcium acetate for treatment. It should be kept in mind that calcium acetate, a food additive, may cause this in patients with the complaint of isolated tongue swelling, but the cause of which cannot be determined

damage in rats

Irinotecan (CPT-11), commonly used in the treatment of many cancer types, may have several side effects that limit the use of CPT-11 in specific tissues such as the heart. In the current study, positive effects of curcumin (CRC) was determined in terms of antioxidant and anti-inflammatory properties against heart damage, caused by CPT-11, in rats. Rats were divided randomly into four equal groups (Control, CPT-11, CRC, and CPT-11 + CRC). CPT-11 10 mg/kg/day was administered intraperitoneally and CRC 100 mg/kg(-1) was given orally. Blood and tissue samples were collected from all groups at day 30 for the detection of oxidative stress, histological changes, and cytokine levels. Results showed that CPT-11 caused dramatic changes in heart tissue for oxidative stress parameters (TBARS, SOD, CAT, GSH, and GPx levels), histological tissue damage, and cytokine levels (TNF and IL-4). CRC therapy reversed the elevated oxidative stress, histological tissue damages, and immunological changes and protected cardiac tissue against CPT-11 toxicity when given together with CPT-11.In conclusion, CPT-11 caused adverse effects on cytokine levels, histological alterations, and oxidative stress in rats. However, CRC treatment eliminated these toxic effects with its antioxidant and anti-inflammatory properties. Thus, these results suggest that CRC may play a protective role against CPT-11 toxicity in heart tissue of rats

and histopathological damage in heart tissue of rats

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant which causes severe toxic effects. Despite there is some suggestion concerning with TCDD induced cardiotoxicity such as formation of free radicals, the main mechanism has not been entirely explained. Beta-glucan is known as strong antioxidant matter and can scavenge free radicals. Therefore this study aimed to investigate the protective effects of beta-glucan against TCDD induced cardiotoxicity in rats. In this study, 2-3 months of age and 190-250 g in weight 32 rats were randomly divided into four equal groups (n=8 for each group). Group 1 was control; Group 2 was TCDD group (2 mu g/kg/week); group 3 was the beta-glucan group(50 mg/kg/day), and group 4 was TCDD and beta-glucan treatment group. The heart samples were taken from rats after 21 days treatment. The results were shown that Despite TCDD exposure visibly caused to increase (p <= 0.001) in TBARS levels, It caused a visible decline in the levels of GSH, CAT, GSH-Px, and SOD. However Beta glucan significantly increased GSH, CAT, GSH-Px, SOD levels and decreased generation of TBARS. Additionally, our histopathological observations were in agreement with the biochemical results. In conclusion, Beta-glucan treatment exhibited protective activity on TCDD induced cardiotoxicity

The beneficial effects of 18β-glycyrrhetinic acid on the experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mouse model.

AIM: The aim of this study was to investigate the beneficial effects of 18β-glycyrrhetinic acid (GA) on the experimental allergic encephalomyelitis (EAE) in C57BL/6 mice. GA is a natural substance found in the root of licorice and is used in traditional Chinese medicine. It has many pharmacological activities such as antioxidant, anti-inflammatory, and anti-cancer effects. MATERIALS AND METHODS: A total of 40 C57BL/6 mice were divided equally into four groups: (1) Control, (2) EAE, (3) GA and (4) GA + EAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, mice were treated with GA at doses of 100 mg/kg/day for 7 days intraperitoneally. RESULTS: To our results, oxidative stress and lipid peroxidations (elevated TBARS levels, decreased GPx, SOD, CAT, and GSH levels) were significantly (p < .01) increased, causing EAE in brain tissue. Also, histopathological damage (Caspase-3 and IL-17 activity, p ≤ .01) and cytokine levels (TNF-α and IL-1β, p < .01) were induced with EAE in mice brain tissue. On the other hand, GA treatment significantly (p < .01) reversed oxidative histological and immunological alterations caused by EAE. CONCLUSIONS: In conclusion, the GA treatment can protect the brain tissue against EAE in mice with its antioxidant and anti-inflammatory properties

experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mouse model

Aim: The aim of this study was to investigate the beneficial effects of 18 beta-glycyrrhetinic acid (GA) on the experimental allergic encephalomyelitis (EAE) in C57BL/6 mice. GA is a natural substance found in the root of licorice and is used in traditional Chinese medicine. It has many pharmacological activities such as antioxidant, anti-inflammatory, and anti-cancer effects.Materials and methods: A total of 40 C57BL/6 mice were divided equally into four groups: (1) Control, (2) EAE, (3) GA and (4) GAthornEAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, mice were treated with GA at doses of 100 mg/kg/day for 7 days intraperitoneally.Results: To our results, oxidative stress and lipid peroxidations (elevated TBARS levels, decreased GPx, SOD, CAT, and GSH levels) were significantly (p<. 01) increased, causing EAE in brain tissue. Also, histopathological damage (Caspase-3 and IL-17 activity, p <=.01) and cytokine levels (TNF-alpha and IL-1 beta, p<. 01) were induced with EAE in mice brain tissue. On the other hand, GA treatment significantly (p<. 01) reversed oxidative histological and immunological alterations caused by EAE.Conclusions: In conclusion, the GA treatment can protect the brain tissue against EAE in mice with its antioxidant and anti-inflammatory properties

reproductive damage

Phthalates that people are exposed to every day are toxic carcinogenic chemicals with proven harmful effects on growth and reproduction. Ellagic acid (EA) is a polyphenol derivative known for its antioxidant properties. We hypothesized that the possible reproductive damage mechanism of phthalates is oxidative attack and ellagic acid could have a protective effect against radical forms in the body through its antioxidant properties. Thirty-two male rats were randomly divided into 4 groups, with 8 rats in each. Phthalate (DBP) was administered intraperitoneally and EA acid through gastric oral gavage (phthalate group 500 mg/kg/day DBP; EA group 2 mg/kg/day ellagic acid; the treatment group 500 mg/kg/day DBP and 2 mg/kg/day EA). The vehicle of DBP and EA, carboxymethyl cellulose was administered to control group. At the end of 4 weeks the testis tissue samples were taken under mild anesthesia. Tissue malondialdehyde, antioxidant parameters, sperm motility, sperm density and abnormal spermatozoon ratios were determined. Analysis was performed with One Way ANOVA test using SPSS 12.0 program. As a result; it has been shown that DBP causes oxidative damage by increasing the malondialdehyde level and decreasing antioxidant parameters, increased abnormal sperm rate and decreased sperm motility and concentration and histopathological damage so this damage is inhibited by the antioxidant activity of ellagic acid.C1 [Turkmen, Nese Basak] Univ Inonu, Fac Pharm, Dept Pharmaceut Toxicol, Malatya, Turkey.[Ayhan, Idris] Ankara Yildirim Beyazit Univ, Fac Med, Dept Med Pharmacol, Ankara, Turkey.[Taslidere, Asli] Univ Inonu, Fac Med, Dept Histol & Embryol, Malatya, Turkey.[Aydin, Muhterem] Firat Univ, Fac Vet Med, Dept Reprod & Artificial Inseminat, Elazig, Turkey.[Ciftci, Osman] Univ Pamukkale, Fac Med, Dept Pharmacol, Denizli, Turkey

Assessment of the Biocompatibility of Mineral Trioxide Aggregate, Bioaggregate, and Biodentine in the Subcutaneous Tissue of Rats

Objective: The objective of this study was to evaluate the tissue inflammation caused by three endodontic repair materials.Materials and Methods: The materials included micro mega‑mineral trioxide aggregate (MM‑MTA), bioaggregate (BA), and biodentine (BD), which were implanted into the subcutaneous tissue of rats. The tissue samples for histological examination were prepared. The infiltration of lymphocytes and macrophages into the tissue was examined to assess the inflammatory response.Results: Lymphocyte infiltration: A significant increase was detected in the MM‑MTA and BA groups on the 7th and 14th days as compared with the control (7th day P = 0.0001, 14th day P = 0.0176). There was no difference between the groups on the 45th day (P = 0.1730). Lymphocyte infiltration had decreased over time in all groups. Macrophage infiltration: There was a significant increase by the 7th day in the test groups as compared to the control group (P = 0.007). However, there was no difference between the experimental groups on the 14th (P = 0.2708) and 45th (P = 0.1291) days.Conclusion: While MM‑MTA and BA showed a similar biocompatibility, BD was more biocompatible than MM‑MTA and BA in the 1st week of the experiment. However, there was no difference between the materials at the end of the 45th day. MM‑MTA, BA, and BD can be considered suitable endodontic repair materials.Keywords: Bioaggregate, Biocompatible Materials, Biodentine, Endodontic

Effects of Ozone Therapy on Cyclophosphamide-induced Urinary Bladder Toxicity in Rats

Purpose: This study investigated the efficacy of ozone therapy (OT) in a rat model of cyclophosphamide-induced hemorrhagic cystitis (HC). Methods: Forty Wistar Albino male rats were divided into five groups: sham, OT, cyclophosphamide (CP), OT+CP and CP+OT. Hemorrhagic cystitis (HC) was induced by intraperitoneal (i.p) administration a single dose of 100 mg/kg CP. OT was performed once daily for three days. The CP+OT group received OT (0.2 mg/kg) i.p 24 h after CP administration. CP was injected to the OT+CP group the day after the third course of OT. All animals were killed four days after CP administration. Bladder injury and oxidative stress parameters were determined from tissue samples. Results: We found small, but non-statistically significant biochemical and histological changes in the animals treated with OT alone. CP administration induced cystitis, as manifested by a marked loss of urothelial cells, as well as hemorrhaging and edema in the bladder as determined by histopathological examination. It also caused a significant decrease in the endogenous antioxidant compound glutathione (GSH) and elevation of lipid peroxidation, and nitric oxide (NO) and myeloperoxidase (MPO) levels in the rats’ urinary bladder tissue. OT was able to ameliorate these changes; however these effects were prominent in the CP+OT group when compared with the OT+CP group.: For example, the NO level in the CP+OT group was 68% of the OT+CP group (p < 0.05). Conclusion: OT prevented CP-induced urothelial damage by diminishing bladder oxidative stress, inflammation and NO levels. OT may help to ameliorate bladder damage induced by CP in the clinical setting