Capsule endoscopy reviewed by a nurse: is it here to stay?
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Capsule Endoscopy↗
Biomedical subjects
J M Herrerías
Publications and source records attributed to J M Herrerías.
Recurrence of Helicobacter pylori infection after several eradication therapies: long-term follow-up of 1000 patients.
AIM: To study the incidence of Helicobacter pylori recurrence, its chronological aspects, and the variables that might influence it. METHODS: A total of 1000 patients in whom H. pylori had been eradicated were prospectively studied. Therapies were classified as low and high efficacy regimens. Four to eight weeks after completion of therapy, 13C-urea-breath-test was performed, and it was repeated yearly up to 5 years. In some patients, endoscopy with biopsies was also performed to confirm H. pylori eradication. RESULTS: A total of 1000 patients were included, giving 2744 patient-years of follow-up. Seventy-one H. pylori recurrences were observed (2.6% per patient-year). Probability of being H. pylori-negative at 1 year was 94.7%, and at 5 years 90.7%. In the multivariate analysis, low age (OR: 1.84; 95% CI: 1.04-3.26) and low efficacy therapies (OR: 2.5; 1.23-5.04) correlated with 1-year H. pylori recurrence. Differences were observed when Kaplan-Meier curves were compared depending on age and therapy regimen. CONCLUSION: Risk of posteradication H. pylori recurrence is higher during the first year, which suggests that most recurrences during this period are recrudescence and not true reinfections. H. pylori recurrence is more frequent in younger patients and in those treated with low efficacy therapies, but is exceptional if high efficacy therapies are used, in which case post-therapy eradication can be safely confirmed at 4 weeks with 13C-urea-breath-test.
Amoxicillin↗
Modification of pepsinogen I levels and their correlation with gastrointestinal injury after administration of dexibuprofen, ibuprofen or diclofenac: a randomized, open-label, controlled clinical trial.
OBJECTIVE: To assess the effect of a 2-week treatment with dexibuprofen, in comparison with ibuprofen and diclofenac, on pepsinogen plasma concentrations and gastrointestinal mucosa, as well as the correlation of these changes with gastrointestinal mucosal injury. METHODS: 60 patients with rheumatologic disease in chronic therapy with NSAID, were included. After a 7-day run-in period patients were randomly assigned to receive a 14-day treatment with dexibuprofen (Group A; Day 1 - 3 = 400 mg t.i.d; Day 4 - 14 = 400 mg b.i.d.), ibuprofen (Group B; Day 1 - 3 = 800 mg t.i.d; Day 4 -14 = 800 mg b.i.d.) or diclofenac (Group C; Day 1 - 3 = 50 mg t.i.d; Day 4 - 14 = 50 mg b.i.d.). Upper gastrointestinal endoscopy (Day 15), capsule-endoscopy (Day 16, 7 patients of each group) and determination of pepsinogen plasma concentrations were performed (basal and Day 15). A semiquantitative scale was designed for the assessment of the gastrointestinal mucosa. RESULTS: No differences in plasma pepsinogen were found between treatment groups or gastrointestinal injury grades or between basal and post-therapy determinations. Dexibuprofen showed gastroduodenal mucosal injury in fewer patients (42.1%) than was the case with ibuprofen (5%; p = 0.003) and diclofenac (30%; p = N.S.). Dexibuprofen administration was also associated with more patients having no intestinal mucosal damage (42.86% vs. 28.7% in the diclofenac group and 14.29% in the ibuprofen group; p = 0.0175). The rate of clinical adverse events was similar in Groups A, B and C (28%, 38% and 34%). CONCLUSIONS: Dexibuprofen showed a lower rate of gastroduodenal and intestinal mucosal injury. This effect was not mediated by modifications of plasma pepsinogen levels.
Administration, Oral↗
The value of capsule endoscopy in pediatric patients with a suspicion of Crohn's disease.
BACKGROUND AND STUDY AIMS: The aim of this study was to assess the safety and usefulness of capsule endoscopy (CE) in pediatric patients with a suspicion of Crohn's disease. PATIENTS AND METHODS: CE was used in 12 patients (four girls, eight boys; age 12-16; weight range 43-87 kg). The indication was a clinical suspicion of Crohn's disease not confirmed with traditional methods. Gastroscopy, colonoscopy, and small-bowel follow-through examinations were carried out in all of the patients, without any diagnostic findings. Ileoscopy was possible in 50 % of the patients, and the ileal mucosa and biopsies were normal in all cases. RESULTS: The capsule was easily swallowed by all of the patients. They all excreted the capsule normally, and no complications were observed in any case. CE identified lesions suggestive of Crohn's disease in seven of the 12 (58.3 %), and the majority of the lesions were in the ileum. CONCLUSIONS: CE is safe in pediatric patients over 12 years of age. The procedure appears to be a very useful diagnostic tool in children with Crohn's disease.
Adolescent↗
Role of L-arginine in ibuprofen-induced oxidative stress and neutrophil infiltration in gastric mucosa.
It has been proposed that neutrophil and oxygen dependent microvascular injuries may be important prime events in gastrointestinal (GI) toxicity of non-steroidal antiinflammatory drugs (NSAIDs). L-arginine (L-ARG) is an essential amino acid which participates in many important biochemical reactions associated to the normal physiology of the organism. In these experimentations, we studied the role of L-ARG, aminoacid precursor of NO synthesis, on ibuprofen (IB) induced gastric lesions, and also on the inflammatory and oxidative mechanisms related to mucosal damage. Oral administration of IB (100 mg kg(-1)), produced severe damage on gastric mucosa, which was more important after 6 h test-period, and was accompanied by a significant increment in myeloperoxidase (MPO) activity, as index of neutrophil activation, as well as lipid peroxidation (LP) levels and xanthine oxidase (XO) activity. However, no changes were observed in total mucosal glutathione (tGSH), nor glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity. Simultaneous treatment with equimolar doses of L-ARG (oral and i.p.), considerably reduced the number and intensity of lesions, and at the same time (6 h) the maximum protection was also observed. In addition, L-ARG inhibited the IB-induced LP and XO enhancement, but did not produce changes in leukocyte infiltration, tGSH, GSH-Px and SOD activity. These findings suggest that (1) L-ARG protective effect on gastric mucosa against IB-induced mucosal lesions could be explained by a local effect and also might be due to the systemic action of the aminoacid; (2) the active oxygen species, derived both from XO and activated neutrophils, could play a role in the pathogenesis of gastric injury induced by IB, (3) L-ARG exhibit a protective effect against IB-induced mucosal damage, probably through the inhibition of oxidative stress derived via xanthine-XO, but it does not block the oxygen free radical production through polymorphe nuclear leukocytes.
Animals↗
Usefulness of capsule endoscopy in patients with suspected small bowel disease.
AIM: To study the usefulness and safety of capsule endoscopy as a diagnostic tool in various small bowel disorders. DESIGN: A retrospective analysis of a series of cases. MATERIAL AND METHODS: Between August 2001 and August 2002, 92 capsule endoscopy procedures were performed in 88 patients (53M/39F, age: 43.87 +/- 16.78). Indications included: chronic diarrhea (n=33); unknown abdominal pain (n=29); occult gastrointestinal bleeding or iron-deficiency anemia (n=13); abdominal discomfort in NSAID takers (n=7); staging of gastrointestinal tumors (n=4), and asymptomatic controls (n=2). Previously performed gastroscopy, colonoscopy, and small-bowel follow-through were not conclusive in all patients. RESULTS: Most frequently relevant findings included: jejuno-ileal aphtas and ulcerations (29 patients), vascular malformations (13 patients), and intestinal neoplasm (6 patients). The groups with a higher rate of findings related to this indication were occult gastrointestinal bleeding (76.92%) and chronic diarrhea (67.85%), with the lowest rate in the abdominal pain group (34.48%). Therapeutic strategy was directly changed in 36 of 88 patients (40.90%) because of capsule-endoscopic findings. The only observed complication was the failed excretion of one of the capsules because of an unknown ulcerated intestinal stricture. CONCLUSIONS: Capsule endoscopy is a safe procedure which can study the entire small bowel, meaning a valuable tool for the management of patients with suggestive signs and symptoms of intestinal disorders.
Adolescent↗
Capsule endoscopy in patients with suspected Crohn's disease and negative endoscopy.
BACKGROUND AND STUDY AIMS: The aim of the present study was to assess the value of capsule endoscopy in the diagnostic work-up of patients in whom there is a clinical suspicion of small bowel Crohn's disease that cannot be confirmed using traditional techniques. PATIENTS AND METHODS: A total of 21 patients (14 men, seven women; mean age 43 +/- 8 years) with a clinical and biochemical suspicion of Crohn's disease were included in the study. Conventional imaging work-up, including upper and lower endoscopy, as well as a small-bowel follow-through, was carried out in all of the patients. RESULTS: Pathological findings were not observed in 12 of the 21 patients (57 %). In the other nine patients (43 %), lesions supporting the diagnosis of Crohn's disease were seen. The most frequent findings were located in the distal ileum and included aphthae, lineal and serpiginous ulcers, and fissures. Four patients had lesions in the jejunum. One patient showed erosions in the distal duodenum, jejunum, and ileum. No adverse effects of the technique were observed in any of the patients. CONCLUSIONS: Capsule endoscopy is a valuable diagnostic tool in patients with suspected Crohn's disease that has not been confirmed using standard imaging techniques.
Adult↗
Short- and medium-term clinical efficacy of three endoscopic therapies for achalasia: a single-blinded prospective study.
OBJECTIVE: to compare the efficacy of three endoscopic therapies for achalasia and to identify predictors of response. DESIGN: prospective, single-blinded study at short and medium term. MATERIAL AND METHODS: 22 patients (9M/13 F; mean age: 47.45 +/- 21.01 years) with confirmed clinical and manometric achalasia were randomised in three groups: intrasphincteric injections of botulinum toxin (group 1: 10 patients ), injections of 1% polidocanol (group 2:6 patients), and a combined therapy with both of them (group 3: 6 patients). Clinical response was evaluated by a score (0-5) of tested symptoms (dysphagia, regurgitation and chest pain) at 1 and 24 weeks post-treatment. RESULTS: at 24 weeks post-treatment group 2 had the best complete response (CR) rate (33.33%), whereas CR in both the botulinum toxin and combined therapy groups was 10 and 0%, respectively. Groups 1 and 2 got an overall improvement in clinical score at 1 (p= 0.02) and 24 weeks (p= 0.04). Five patients (50%) in group 1, two patients (33.33%) in group 2, and three patients (50%) in group 3 needed other therapies (dilation or surgery) because of treatment failure. Separately, neither age nor sex, time from diagnosis or type of therapy could distinguish responders from non-responders in these three groups. However, absence of response within the first week, and an initial clinical score above 7 were predictive factors of poor response at six months. CONCLUSIONS: short- and medium-term clinical response to these endoscopic therapies was limited. The absence of response at seven days and a severe initial clinical score were predictive factors of poor medium-term response.
Adult↗
Gastric toxicity of racemic ketoprofen and its enantiomers in rat: oxygen radical generation and COX-expression.
OBJECTIVE AND DESIGN: The gastric toxicity of racemic-ketoprofen and its enantiomers (S(+)- and R(-)-ketoprofen), oxygen free radical generation and neutrophil infiltration in response to damage were evaluated in rats. Changes in prostaglandin synthesis, cyclooxygenase expression and glutathione metabolism were also studied. MATERIALS AND METHODS: Studies were performed in Wistar rats. Drugs were given by oral administration: racemic-ketoprofen (100, 50 and 25 mg/kg body weight); S(+) and R(-)-ketoprofen (50, 25 and 12.5 mg/kg body weight). Determinations were made of gastric mucosal injury, lipid peroxidation, xanthine oxidase, myeloperoxidase and superoxide dismutase activities, glutathione levels, glutathione peroxidase and glutathione reductase activities, gastric prostaglandin synthesis (PGE2 levels) and COX-expression. RESULTS: Racemic-ketoprofen dose-dependently exhibited the highest toxicity. In contrast, S(+)-ketoprofen at half the dose of the racemic compound proved to be less ulcerogenic. R(-)-ketoprofen was also less ulcerogenic, but when administered as the racemate exacerbated gastric ulceration caused by S(+)-ketoprofen. Drug administration produced significant increases in lipid peroxidation levels and xanthine-oxidase and a decrease in superoxide dismutase activity. Nevertheless the racemate induced the highest disturbances in oxidative metabolism. No changes in myeloperoxidase values and glutathione metabolism were found. Cyclooxygenase-1 immunoreactivity was observed and did not differ from that in control rats. Cyclooxygenase-2 could also be expressed after treatments. CONCLUSIONS: R(-)-ketoprofen and S(+)-ketoprofen have a comparable gastric toxicity and they both have a better gastric toxicity profile as compared to the racemate. In addition to inhibition of prostaglandin synthesis, damage resulted in an increase of cyclooxygenase-2 protein expression. Oxygen radicals, including superoxide anions, could also be implicated.
Animals↗
Role of prostaglandins and nitric oxide in gastric damage induced by metamizol in rats.
OBJECTIVE AND DESIGN: In addition to the depletion of prostaglandins (PGs), oxygen free radicals generation and nitrogen species haven been implicated in non-steroidal anti-inflammatory drugs (NSAIDs)-induced gastric injury. The aim of the present study was to examine changes in PGE2 generation and its relationship with proinflammatory parameters and nitric oxide (NO) production in the comparative pathogenesis of gastric injury induced by metamizol vs. diclofenac, NSAIDs that present different gastric tolerability and cyclooxygenase (COX) inhibition profiles. MATERIAL: Studies were performed in Wistar-Han rats. TREATMENTS: Metamizol (120, 500 and 1,000 mg/kg body weight) and diclofenac (50 mg/kg body weight) were given by oral administration. METHODS: Determinations were made of macroscopic and histological evaluation of gastric mucosal injury, gastric prostaglandin synthesis (PGE2 levels), myeloperoxidase activity (MPO), tumor necrosis factor-alpha levels (TNF-a), cyclic guanosine monophosphate (cGMP), nitric oxide synthase activity (NOS) and NOS mRNA expression. RESULTS: Metamizol, only at the highest doses assayed, provoked weak lesions in the gastric mucosa. To the contrary, diclofenac treatment presented the highest grade of lesion. All treatments decreased PGE2 gastric generation. Treatment of the animals with metamizol neither modified the MPO activity nor TNF-alpha levels. In contrast, statistically significant increases in both parameters were observed after diclofenac administration. cGMP levels were not influenced with diclofenac treatment, nevertheless metamizol reduced the nucleotide levels, which was accompanied by an inhibition of constitutive NOS (cNOS) activity without modifying the mRNA expression of the enzyme. CONCLUSIONS: In addition to inhibition of PG synthesis, damage induced by metamizol was associated with an inhibition of the NO/cGMP pathway and cNOS activity. In contrast, diclofenac-induced gastric damage was associated with an increase of the inflammatory response.
Animals↗
[Endoscopic treatment of pain in patients with chronic pancreatitis].
INTRODUCTION: Chronic Pancreatitis is a recurrent disease, frequently alcohol intake related and tend to occur in the third and the fourth decades. Stenoses and lithiasis in the main pancreatic duct causes obstruction and subsequently pain. Therefore endoscopic or surgical decompression of main pancreatic duct results in pain relief. SUBJECTS AND METHODS: Review our experience in the endoscopic management in patients suffering from chronic pancreatitis. 42 patients underwent ERCP for management of their chronic pancreatitis. Therapeutic options were sphincterotomy alone, prostheses and "do nothing". Follow-up was made by phone call and outpatient office visits. Mean follow-up was 47.8 (27.2) months. RESULTS: 22 patients underwent therapeutic ERCP. In 8 patients we performed sphincterotomy and in 14 patients, a sphincterotomy and prostheses intubation. 8 patients are asymptomatic after a mean follow-up of 10.8 (11.6) months. 2 of them, underwent sphincterotomy and six of them, underwent sphincterotomy and prostheses intubation. CONCLUSION: Therapeutic ERCP is a tool that relieves pain in a fifth of patients suffering from chronic pancreatitis.
Adolescent↗
Posterior laryngitis: effects of treatment with omeprazole alone.
OBJECTIVE: To evaluate the effect of omeprazole treatment on the symptoms and lesions of patients with posterior laryngitis (PL). PATIENTS AND METHOD: Twenty-one patients with a clinical and laryngoscopic diagnosis of PL were studied. Results for each laryngeal symptom (dysphonia, hoarseness, cough, foreign body sensation, and burning) and laryngoscopic finding (mucus stasis, erythema, oedema, hypertrophy, ulceration, and granulation) at baseline, 12 weeks after treatment with omeprazole, 20 mg twice daily, and 12 weeks after treatment discontinuation were compared. No changes in their hygienic-dietary or postural habits were recommended. RESULTS: A reduction in symptom severity and frequency was observed (p < 0.05), as well as in the severity of laryngoscopic findings (p < 0.05)--except for granulation--immediately after treatment discontinuation. A relapse of laryngoscopic findings was seen at 12 weeks after treatment discontinuation (p < 0.01). The trend towards symptom recurrence was not significant. CONCLUSION: Treatment with omeprazole alone modifies clinical manifestations and endoscopic findings in patients with PL. Controlled clinical trials with a high number of patients and longer-term follow-up are needed to define the best therapeutic regimen for these patients.
Adult↗
Diagnosis of Helicobacter pylori infection in patients with upper gastrointestinal bleeding due to peptic ulcer.
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Anti-Ulcer Agents↗
Mediterranean diet and health: biological importance of olive oil.
Olive oil, the main fatty component of the Mediterranean diet, is characterized by consisting of monounsaturated fatty acids as well as by its elevated content in antioxidant agents. This oil exhibits numerous biological functions which are beneficial for the state of health. A diet rich in monounsaturated fatty acids provides an adequate fluidity to the biological membranes, diminishing the hazard of lipid peroxidation which affects polyunsaturated fatty acids. Moreover, the antioxidants present in olive oil are able to scavenge free radicals and afford an adequate protection against peroxidation. Regarding the heart, olive oil decreases the plasmatic levels of LDL-cholesterol and increases those of HDL-cholesterol, hence diminishing the risk of suffering from heart complaints. In this context, it has been suggested that increased consumption of monounsaturated fatty acids in place of polyunsaturated fatty acids will render circulating lipoproteins less sensitive to peroxidation and thereby diminish the development of atherosclerosis. Olive oil has also been proven to contribute to a better control of the hypertriglyceridemia accompanying diabetes and may reduce the risk of breast cancer and colorectum. On the other hand, several investigations have suggested that olive oil can be beneficial in inflammatory and autoimmune diseases, such as rheumatoid arthritis. In this sense, some reports have indicated that olive oil modifies inflammatory cytokines production. As for the digestive system, olive oil enhances gallbladder emptying consequently reducing cholelithiasis risk, decreases the pancreatic exocrine secretion and gastric secretory function in response to food. Finally, it has been demonstrated that a diet rich in olive oil is associated with a high percentage of gastric ulcer healing and affords a higher resistance against non steroidal antiinflammatory drugs-induced gastric ulcerogenesis.
Cholesterol↗
Antiinflamatory agents less dangerous for gastrointestinal tract.
NSAIDs represent one of the most commonly used therapeutic drug groups world wide. 1.5% of the world's population is estimated as taking NSAIDs. However, their use is not risk free and gastrointestinal (GI) lesions do appear, which is indeed the main reason for their toxicity. Frequently (50%) NSAID-induced GI lesions are asymptomatic, and perforations or hemorrhages could occur without any previous symptoms. 71% of GI perforations and 50% of upper gastric hemorrhages (UGH) are associated with taking NSAIDs. How frequent GI lesions appear is directly related to whether the patient is in a risk group or not. Factors increasing the risk of GI lesions occurring are the following: being older than 60, using corticoids or other NSAIDs concomitantly, having a history of duodenal ulcer, alcohol consumption, smoking or taking oral anticoagulants. As the toxicity and how frequent the lesions appear depend on which drug is used, there is a need for research into new drugs which are both clinically effective and safer to use. GI toxicity of NSAIDs is mediated by two mechanisms, direct toxicity and prostaglandin synthesis inhibition or sistemic mechanism. Due to the relatively recent discoveries concerning the physiopathology of inflammation and gastric physiology, research into new NSAID derivatives is taking place. Such derivatives are prodrugs, galenic buffer forms, selective COX-2 inhibitors, isomeric compounds, NO-donors, and as a future possibility, phosphodiesterase inhibitors.
Animals↗
Long-term management of GERD. Why using endoscopy just now?
Early results with the use of endoscopic techniques in the treatment of gastro-oesophageal reflux disease (GERD) have been recently reported. Methods used are an injection of biocompatible substances within the lower oesophageal sphincter (LES), LES ablation using radio-frequency, and suture of folds in the area distal to the Z-line. The latter--endoscopic gastroplasty--is most difficult, but this technique has been most widely accepted by gastroenterologists to this date. Effectiveness of these endoscopic management systems in the long-term control of GERD has never been compared to a control group. This fact, together with the proven efficacy of anti-secretory drugs and the refinement of laparoscopic surgery during the past few years, has led physicians to be more demanding regarding early results. This review will discuss each method available, and issues answered by reported studies to this day are approached.
Biocompatible Materials↗
Intestinal toxicity of ketoprofen-trometamol vs its enantiomers in rat. Role of oxidative stress.
OBJECTIVE: Gastrointestinal damage and bleeding are the major side effects of non-steroidal anti-inflammatory drugs (NSAID), however the mechanisms of this ulcerogenic action are not fully understood. It has recently been proposed that neutrophil-and oxygen radical-dependent microvascular injuries may be important prime events that lead to mucosal injury. In addition, other factors like bile flow, intact bacterial flora or feeding conditions may contribute to the formation of lesions. Ketoprofen is a NSAID that exists as a pair of R(-) and S (+) enantiomers; like other 2-arylpropionic acids, its anti-inflammatory effects resides almost exclusively in the S (+) isomer. The present study was undertaken to explore the role of oxidative stress in the pathogenesis of intestinal injury induced by oral administration of racemic ketoprofen and its enantiomers given as their water soluble tromethamine salts. MATERIAL AND METHODS: Evaluation of intestinal damage and activities of oxidative stress related enzymes such as myeloperoxidase (MPO), xanthine-oxidase (XO) and superoxide dismutase (SOD) were studied in an experimental animal model using refed rats. RESULTS: After the oral treatment followed by a refeeding period of 24 h, ketoprofen (100, 50, 25 mg/Kg b.w.) dose-dependently caused longitudinal ulcers on the mesenteric side of the middle and lower intestine lumen. The intestinal toxicity caused by S(+)-ketoprofen was significantly lower than the effect observed after racemate and R(-) enantiomer treatments (P <0.001), though the bioinversion of R(-)-ketoprofen to S(+)-enantiomer that occurs in the rat has to be considered. XO activity was unaffected by the studied drugs. Enhanced enteropathy by the racemate and its R (-)-enantiomer was correlated with a significant increase of MPO activity as an index of neutrophil infiltration, and a decrease in SOD activity (p<0.05 Vs control). S(+)-ketoprofen did not significantly change these parameters. CONCLUSIONS: These results suggest that reactive oxygen metabolites can contribute significantly to the development of intestinal lesions, and that R(-)-ketoprofen present in racemic preparations can enhance the toxic intestinal effects of S (+)-enantiomer via modification of neutrophil migration and oxidative stress.
Administration, Oral↗
Protective effect of melatonin on indomethacin-induced gastric injury in rats.
The gastric injury associated with nonsteroidal anti-inflammatory drug (NSAID) therapy has been linked to the detrimental effects of the agents on the processes of prostaglandin synthesis, neutrophil (PMN) activation. and oxygen free radical generation. In the present study, we investigated the in vivo protective effects of melatonin on indomethacin-induced gastric lesions in the rat. Peroxidation of lipids and changes in the activities of related enzymes such as glutathione peroxidase (GSH-px) and myeloperoxidase (MPO), as a marker of PMNs infiltration, were also studied. Intraperitoneal (i.p.) injection of melatonin (0.25. 0.5, 1 mg kg(-1)) 30 min before indomethacin administration prevented gastric injury. The mean ulcer indices significantly (P < 0.05) decreased. Thiobarbituric acid (TBA) reactive substances in the gastric mucosa as an index of peroxidation, was increased after indomethacin administration and this increase was inhibited by melatonin. In addition, pretreatment with melatonin resulted in a significant increase of the enzymatic GSH-px activity up to the control levels; however, inhibition of ulceration by melatonin was not associated with a significant reduction in PMN infiltration. These results suggest that the protection afforded by the pineal hormone against indomethacin-induced gastric injury may be, in addition to other possible mechanisms, to its radical scavenging activity.
Animals↗