Propolis Modulates Inflammatory Mediators and Improves Histopathology in Male Rats with L-arginine-induced Acute Pancreatitis.

OBJECTIVES: This study aimed to determine the effects of propolis on immune mediators and tissue histopathology in rats with L-arginine-induced acute pancreatitis (AP). METHODS: This study was conducted at Imam Abdulrahman Bin Faisal University, Dammam, Saudia Arabia between September and November 2017. A total of 24 male albino Wistar rats were divided into three equal groups. Group one was the negative control, group two was the positive control (L-arginine-induced AP) and group three received treatment (L-arginineinduced AP and propolis). The rats in group three were treated with 100 mg/kg propolis for seven days after AP induction. Pancreatic tissue was evaluated histologically and levels of interleukin (IL)-6, IL-22 and IL-1ß and tumour necrosis factor-alpha (TNF-α) were measured. RESULTS: Propolis reduced the quanitity of proinflammatory molecules (TNF-α, IL-1ß and IL-6) in group three compared to group two, significantly increased the overall anti-inflammatory effect of IL-22 (P <0.005) and reduced interstitial inflammation and neutrophil cell infiltration of the pancreatic tissues. CONCLUSION: Propolis may exert a therapeutic effect in AP. Further studies are required to demonstrate the mechanisms of propolis in AP.

Arginine intake is associated with oxidative stress in a general population.

OBJECTIVE: The aim of this study was to assess the association between protein and arginine from meat intake and oxidative stress in a general population. METHODS: Data came from the Health Survey for Sao Paulo (ISA-Capital), a cross-sectional population-based study in Brazil (N = 549 adults). Food intake was estimated by a 24-h dietary recall. Oxidative stress was estimated by malondialdehyde (MDA) concentration in plasma. Analyses were performed using general linear regression models adjusted for some genetic, lifestyle, and biochemical confounders. RESULTS: MDA levels were associated with meat intake (P for linear trend = 0.031), protein from meat (P for linear trend = 0.006), and arginine from meat (P for linear trend = 0.044) after adjustments for confounders: age, sex, body mass index, smoking, physical activity, intake of fruit and vegetables, energy and heterocyclic amines, C-reactive protein levels, and polymorphisms in GSTM1 (glutathione S-transferase Mu 1) and GSTT1 (glutathione S-transferase theta 1) genes. Results were not significant for total protein and protein from vegetable intake (P > 0.05). CONCLUSIONS: High protein and arginine from meat intake were associated with oxidative stress independently of genetic, lifestyle, and biochemical confounders in a population-based study. Our results suggested a novel link between high protein/arginine intake and oxidative stress, which is a major cause of age-related diseases.

Biomarkers of arginine and lysine excess.

Arginine supplementation is used in several disease states. In arginine-deficient states, supplementation is a logical choice of therapy. However, the definition of an arginine-deficient state is complex. For example, plasma arginine levels could be within normal range but intracellular arginine levels could be reduced because of membrane transport problems. Lysine competes with arginine for transport into the cell. In these situations, arginine supplementation of higher than required levels is proposed. Arginine has several important functions in metabolism as it is a precursor of metabolically active components such as nitric oxide (NO), ornithine, creatine, and polyamines. Supplementing arginine in excess could potentially overstimulate metabolism via enhanced production of NO. NO is a reactive component that, via production of radicals, will inactivate proteins. NO is also a powerful vasodilator, which could lead to severe hemodynamic instability. A good marker for excess supplementation of arginine or lysine could be an increased or reduced production rate of NO. However, NO production is difficult to measure because NO is a very labile component and is rapidly oxidized in blood. Stable isotope-labeled arginine and citrulline are used to trace the arginine-NO route. During supplementation of arginine in septic pigs or patients in septic shock, NO production, measured with stable isotope technology, is enhanced.

A fatal overdose of arginine hydrochloride.

CASE REPORT: Arginine hydrochloride is used both diagnostically to test for growth hormone deficiency and therapeutically for treatment of metabolic alkalosis. We describe a 21-month-old girl who developed cardiopulmonary arrest following an accidental overdose of arginine hydrochloride. The patient developed acute metabolic acidosis and transient, but severe, hyponatremia. Thirty-six hours after successful resuscitation, she developed fatal central pontine and extrapontine myelinolysis. Unlike previous reports of arginine-toxicity, our patient showed no evidence of hyperkalemia. This case illustrates a previously unreported mechanism of arginine hydrochloride toxicity.