A Scrupulous Overview on Controlled Release Fertilizers

ABSTRACT With the increase in the world population and the demand for food, new agricultural practices have been developed to improve food production through the use of more effective pesticides and fertilisers. Controlled release technology is an invaluable scientific tool for improving performance and safety of chemicals, which involve materials such a

Estresse oxidativo: conceito, implicações e fatores modulatórios Oxidative stress: concept, implications and modulating factors

O estresse oxidativo decorre de um desequilíbrio entre a geração de compostos oxidantes e a atuação dos sistemas de defesa antioxidante. A geração de radicais livres e/ou espécies reativas não radicais é resultante do metabolismo de oxigênio. A mitocôndria, por meio da cadeia transportadora de elétrons, é a principal fonte geradora. O sistema de defesa antioxidante tem a função de inibir e/ou reduzir os danos causados pela ação deletéria dos radicais livres e/ou espécies reativas não radicais. Esse sistema, usualmente, é dividido em enzimático (superóxido dismutase, catalase e glutationa peroxidase) e não-enzimático. No último caso, é constituído por grande variedade de substâncias antioxidantes, que podem ter origem endógena ou dietética. Objetivou-se revisar os principais mecanismos de geração de radicais livres, bem como a ação dos agentes mais relevantes do sistema de defesa antioxidante, ressaltando suas implicações sobre os marcadores do estresse oxidativo. Também serão abordados os principais fatores exógenos moduladores do estresse oxidativo.<br>There is evidence that oxidative stress, defined as a persistent imbalance between the production of highly oxidative compounds and antioxidant defenses, leads to tissue damage. Oxygen metabolism generates free radicals and/or non-radical reactive oxygen species. The mitochondria, through the electron transport chain, are the main generator of these species. The antioxidant defense system has the function of inhibiting and/or reducing the damage caused by the deleterious free radicals and/or non-radical reactive oxygen species. This system is divided into enzymatic (superoxide dismutase, catalase and glutathione peroxidase), and nonenzymatic. The nonenzymatic system consists of a variety of antioxidant substances, which may be endogenous or dietary. This study proposed to review the main mechanisms of reactive oxygen species generation and the role of the most relevant agents of the antioxidant defense system on the biomarkers of oxidative stress. The main exogenous factors that modulate oxidative stress will also be discussed

Exenatide Treatment Alone Improves β-Cell Function in a Canine Model of Pre-Diabetes

BACKGROUND:Exenatide's effects on glucose metabolism have been studied extensively in diabetes but not in pre-diabetes. OBJECTIVE:We examined the chronic effects of exenatide alone on glucose metabolism in pre-diabetic canines. DESIGN AND METHODS:After 10 weeks of high-fat diet (HFD), adult dogs received one injection of streptozotocin (STZ, 18.5 mg/kg). After induction of pre-diabetes, while maintained on HFD, animals were randomized to receive either exenatide (n = 7) or placebo (n = 7) for 12 weeks. β-Cell function was calculated from the intravenous glucose tolerance test (IVGTT, expressed as the acute insulin response, AIRG), the oral glucose tolerance test (OGTT, insulinogenic index) and the graded-hyperglycemic clamp (clamp insulinogenic index). Whole-body insulin sensitivity was assessed by the IVGTT. At the end of the study, pancreatic islets were isolated to assess β-cell function in vitro. RESULTS:OGTT: STZ caused an increase in glycemia at 120 min by 22.0% (interquartile range, IQR, 31.5%) (P = 0.011). IVGTT: This protocol also showed a reduction in glucose tolerance by 48.8% (IQR, 36.9%) (P = 0.002). AIRG decreased by 54.0% (IQR, 40.7%) (P = 0.010), leading to mild fasting hyperglycemia (P = 0.039). Exenatide, compared with placebo, decreased body weight (P<0.001) without altering food intake, fasting glycemia, insulinemia, glycated hemoglobin A1c, or glucose tolerance. Exenatide, compared with placebo, increased both OGTT- (P = 0.040) and clamp-based insulinogenic indexes (P = 0.016), improved insulin secretion in vitro (P = 0.041), but had no noticeable effect on insulin sensitivity (P = 0.405). CONCLUSIONS:In pre-diabetic canines, 12-week exenatide treatment improved β-cell function but not glucose tolerance or insulin sensitivity. These findings demonstrate partial beneficial metabolic effects of exenatide alone on an animal model of pre-diabetes