Cholinesterase activities and oxidative stress in cattle experimentally exposed to nitrate/nitrite in cultivated pasture with different fertilization schemes

Background: Nitrate and nitrite poisoning is associated with pasture intake that has high nitrate levels and leads to acute methemoglobinemia. Pasture may accumulate nitrate under certain conditions, such as excessively fertilized soil or environmental conditions that enhance the N absorption (rain preceded by a period of drought). After ingestion of plants, this substrate reaches the rumen and, in physiological conditions, is reduced to nitrite and afterward to ammonia. The aim of this study was to evaluate changes in cholinesterase activities and oxidative stress caused by subclinical poisoning for nitrate and nitrite in cattle fed with Pennisetum glaucum in three different fertilization schemes.Materials, Methods & Results: In order to perform the experimental poisoning, the pasture was cultivated in three different paddocks: with nitrogen topdressing (urea; group 1), organic fertilizer (group 2) or without fertilizer (group 3; control). Nitrate accumulation in forage was evaluated by the diphenylamine test. After food fasting of 12 h, nine bovine were randomly allocated to one of the experimental groups and fed with fresh forage (ad libitum) from respective paddock. In different time points from beginning of pasture intake (0, 2, 4, 6 and 9 h) heart rate and respiratory frequency were assessed, as well as mucous membrane color and behavioral changes. Blood samples from jugular vein into vials with and without anticoagulant were collected. From blood samples, serum nitrite levels, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzyme activity were evaluated, as well as oxidative stress through the following parameters: levels of nitrate/nitrite (NOx ), thiobarbituric acid reactive substances (TBARS) and reactive oxygen species (ROS), beyond the antioxidant system by enzyme activity measurement of catalase (CAT) and superoxide dismutase (SOD).[...]

Cholinesterase activities and oxidative stress in cattle experimentally exposed to nitrate/nitrite in cultivated pasture with different fertilization schemes

Background: Nitrate and nitrite poisoning is associated with pasture intake that has high nitrate levels and leads to acute methemoglobinemia. Pasture may accumulate nitrate under certain conditions, such as excessively fertilized soil or environmental conditions that enhance the N absorption (rain preceded by a period of drought). After ingestion of plants, this substrate reaches the rumen and, in physiological conditions, is reduced to nitrite and afterward to ammonia. The aim of this study was to evaluate changes in cholinesterase activities and oxidative stress caused by subclinical poisoning for nitrate and nitrite in cattle fed with Pennisetum glaucum in three different fertilization schemes.Materials, Methods & Results: In order to perform the experimental poisoning, the pasture was cultivated in three different paddocks: with nitrogen topdressing (urea; group 1), organic fertilizer (group 2) or without fertilizer (group 3; control). Nitrate accumulation in forage was evaluated by the diphenylamine test. After food fasting of 12 h, nine bovine were randomly allocated to one of the experimental groups and fed with fresh forage (ad libitum) from respective paddock. In different time points from beginning of pasture intake (0, 2, 4, 6 and 9 h) heart rate and respiratory frequency were assessed, as well as mucous membrane color and behavioral changes. Blood samples from jugular vein into vials with and without anticoagulant were collected. From blood samples, serum nitrite levels, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzyme activity were evaluated, as well as oxidative stress through the following parameters: levels of nitrate/nitrite (NOx ), thiobarbituric acid reactive substances (TBARS) and reactive oxygen species (ROS), beyond the antioxidant system by enzyme activity measurement of catalase (CAT) and superoxide dismutase (SOD).[...](AU)

Rattlesnake Crotalus molossus nigrescens venom induces oxidative stress on human erythrocytes

Background Globally, snake envenomation is a well-known cause of death and morbidity. In many cases of snakebite, myonecrosis, dermonecrosis, hemorrhage and neurotoxicity are present. Some of these symptoms may be provoked by the envenomation itself, but others are secondary effects of the produced oxidative stress that enhances the damage produced by the venom toxins. The only oxidative stress effect known in blood is the change in oxidation number of Fe (from ferrous to ferric) in hemoglobin, generating methemoglobin but not in other macromolecules. Currently, the effects of the overproduction of methemoglobin derived from snake venom are not extensively recorded. Therefore, the present study aims to describe the oxidative stress induced by Crotalus molossus nigrescens venom using erythrocytes. Methods Human erythrocytes were washed and incubated with different Crotalus molossus nigrescens venom concentrations (0-640 μg/mL). After 24 h, the hemolytic activity was measured followed by attenuated total reflectance-Fourier transform infrared spectroscopy, non-denaturing PAGE, conjugated diene and thiobarbituric acid reactive substances determination. Results Low concentrations of venom (<10 μg/mL) generates oxyhemoglobin release by hemolysis, whereas higher concentrations produced a hemoglobin shift of valence, producing methemoglobin (>40 μg/mL). This substance is not degraded by proteases present in the venom. By infrared spectroscopy, starting in 80 μg/mL, we observed changes in bands that are associated with protein damage (1660 and 1540 cm−1) and lipid peroxidation (2960, 2920 and 1740 cm−1). Lipid peroxidation was confirmed by conjugated diene and thiobarbituric acid reactive substance determination, in which differences were observed between the control and erythrocytes treated with venom. Conclusions Crotalus molossus nigrescens venom provokes hemolysis and oxidative stress, which induces methemoglobin formation, loss of protein structure and lipid peroxidation.(AU)

Rattlesnake Crotalus molossus nigrescens venom induces oxidative stress on human erythrocytes

Background Globally, snake envenomation is a well-known cause of death and morbidity. In many cases of snakebite, myonecrosis, dermonecrosis, hemorrhage and neurotoxicity are present. Some of these symptoms may be provoked by the envenomation itself, but others are secondary effects of the produced oxidative stress that enhances the damage produced by the venom toxins. The only oxidative stress effect known in blood is the change in oxidation number of Fe (from ferrous to ferric) in hemoglobin, generating methemoglobin but not in other macromolecules. Currently, the effects of the overproduction of methemoglobin derived from snake venom are not extensively recorded. Therefore, the present study aims to describe the oxidative stress induced by Crotalus molossus nigrescens venom using erythrocytes. Methods Human erythrocytes were washed and incubated with different Crotalus molossus nigrescens venom concentrations (0-640 μg/mL). After 24 h, the hemolytic activity was measured followed by attenuated total reflectance-Fourier transform infrared spectroscopy, non-denaturing PAGE, conjugated diene and thiobarbituric acid reactive substances determination. Results Low concentrations of venom (<10 μg/mL) generates oxyhemoglobin release by hemolysis, whereas higher concentrations produced a hemoglobin shift of valence, producing methemoglobin (>40 μg/mL). This substance is not degraded by proteases present in the venom. By infrared spectroscopy, starting in 80 μg/mL, we observed changes in bands that are associated with protein damage (1660 and 1540 cm−1) and lipid peroxidation (2960, 2920 and 1740 cm−1). Lipid peroxidation was confirmed by conjugated diene and thiobarbituric acid reactive substance determination, in which differences were observed between the control and erythrocytes treated with venom. Conclusions Crotalus molossus nigrescens venom provokes hemolysis and oxidative stress, which induces methemoglobin formation, loss of protein structure and lipid peroxidation.(AU)

Rattlesnake Crotalus molossus nigrescens venom induces oxidative stress on human erythrocytes

Abstract Background Globally, snake envenomation is a well-known cause of death and morbidity. In many cases of snakebite, myonecrosis, dermonecrosis, hemorrhage and neurotoxicity are present. Some of these symptoms may be provoked by the envenomation itself, but others are secondary effects of the produced oxidative stress that enhances the damage produced by the venom toxins. The only oxidative stress effect known in blood is the change in oxidation number of Fe (from ferrous to ferric) in hemoglobin, generating methemoglobin but not in other macromolecules. Currently, the effects of the overproduction of methemoglobin derived from snake venom are not extensively recorded. Therefore, the present study aims to describe the oxidative stress induced by Crotalus molossus nigrescens venom using erythrocytes. Methods Human erythrocytes were washed and incubated with different Crotalus molossus nigrescens venom concentrations (0640 g/mL). After 24 h, the hemolytic activity was measured followed by attenuated total reflectance-Fourier transform infrared spectroscopy, non-denaturing PAGE, conjugated diene and thiobarbituric acid reactive substances determination. Results Low concentrations of venom ( 10 g/mL) generates oxyhemoglobin release by hemolysis, whereas higher concentrations produced a hemoglobin shift of valence, producing methemoglobin (>40 g/mL). This substance is not degraded by proteases present in the venom. By infrared spectroscopy, starting in 80 g/mL, we observed changes in bands that are associated with protein damage (1660 and 1540 cm1) and lipid peroxidation (2960, 2920 and 1740 cm1). Lipid peroxidation was confirmed by conjugated diene and thiobarbituric acid reactive substance determination, in which differences were observed between the control and erythrocytes treated with venom. Conclusions Crotalus molossus nigrescens venom provokes hemolysis and oxidative stress, which induces methemoglobin formation, loss of protein structure and lipid peroxidation.

Nitrate in ruminant feeding mitigates methane production / Nitrato na alimentação de ruminantes mitiga a produção de metano

Methane and carbon dioxide are natural products of microbial fermentation primarily of carbohydrates and lesser extent of amino acids in rumen and intestine of the animals. The main factor affecting methane production in ruminants is the food, due to providing substrate for methanogenic bacteria. Changes in animal nutrition through the use of strategic resources, with a balanced diet based on the physiological needs of animals contributes to the reduction of methane production. Nitrate when added in ruminant diet promotes the use of hydrogen ions for its conversion to ammonia. Some microorganisms are able to reduce nitrate to nitrite and then nitrite to ammonia using hydrogen, and therefore methanogenesis can be reduced. However, the supply of nitrate, without an adaptation period, in levels that exceed the ruminant capacity to use it can lead to the occurrence of methemoglobinemia. To avoid poisoning is recommended an adaptation period of animals to the nitrate content.(AU)  

O metano e o dióxido de carbono são subprodutos naturais da fermentação microbiana principalmente de carboidratos e em menor extensão dos aminoácidos no rúmen e no intestino grosso dos animais. O fator primário que afeta a produção de metano pelos ruminantes é a alimentação, pelo fato de fornecer substrato para as bactérias metanogênicas. Mudanças na alimentação dos animais através do uso estratégico de recursos disponíveis, com uma dieta equilibrada com base nas necessidades fisiológicas dos animais contribui com a redução da produção de metano. O nitrato quando fornecido na dieta de ruminantes promove o uso de íons hidrogênio para sua conversão em amônia. Alguns microrganismos são capazes de reduzir nitrato a nitrito e então nitrito a amônia com o uso de hidrogênio, assim a metanogênese pode ser reduzida. No entanto, o fornecimento de nitrato, em teores excessivos para ruminantes, sem cuidados quanto à adaptação dos animais as dietas, pode levar a ocorrência de metahemoglobinemia. Para evitar a intoxicação recomenda-se que haja adaptação dos animais aos teores de nitrato.(AU)

Nitrate in ruminant feeding mitigates methane production / Nitrato na alimentação de ruminantes mitiga a produção de metano

Methane and carbon dioxide are natural products of microbial fermentation primarily of carbohydrates and lesser extent of amino acids in rumen and intestine of the animals. The main factor affecting methane production in ruminants is the food, due to providing substrate for methanogenic bacteria. Changes in animal nutrition through the use of strategic resources, with a balanced diet based on the physiological needs of animals contributes to the reduction of methane production. Nitrate when added in ruminant diet promotes the use of hydrogen ions for its conversion to ammonia. Some microorganisms are able to reduce nitrate to nitrite and then nitrite to ammonia using hydrogen, and therefore methanogenesis can be reduced. However, the supply of nitrate, without an adaptation period, in levels that exceed the ruminant capacity to use it can lead to the occurrence of methemoglobinemia. To avoid poisoning is recommended an adaptation period of animals to the nitrate content.

O metano e o dióxido de carbono são subprodutos naturais da fermentação microbiana principalmente de carboidratos e em menor extensão dos aminoácidos no rúmen e no intestino grosso dos animais. O fator primário que afeta a produção de metano pelos ruminantes é a alimentação, pelo fato de fornecer substrato para as bactérias metanogênicas. Mudanças na alimentação dos animais através do uso estratégico de recursos disponíveis, com uma dieta equilibrada com base nas necessidades fisiológicas dos animais contribui com a redução da produção de metano. O nitrato quando fornecido na dieta de ruminantes promove o uso de íons hidrogênio para sua conversão em amônia. Alguns microrganismos são capazes de reduzir nitrato a nitrito e então nitrito a amônia com o uso de hidrogênio, assim a metanogênese pode ser reduzida. No entanto, o fornecimento de nitrato, em teores excessivos para ruminantes, sem cuidados quanto à adaptação dos animais as dietas, pode levar a ocorrência de metahemoglobinemia. Para evitar a intoxicação recomenda-se que haja adaptação dos animais aos teores de nitrato.

Intoxicação por paracetamol em gatos / Acetaminophen toxicity in cats

intoxicação por paracetamol em gatos ocorre por exposição acidental ou de forma iatrogênica, quando um responsável o administra na intenção de tratar seu animal. Os gatos apresentam defi ciência em sua biotransformação e por isso mesmo pequenas doses do fármaco podem provocar sinais de intoxicação. Dentre os sinais clínicos pode-se observar cianose, depressão, icterícia, edema de face e membros, taquipnéia, dispnéia, anorexia, fraqueza, vômito, hipotermia e hematúria. Felizmente, com um tratamento agressivo e cuidado de suporte adequado, a maioria dos animais se recupera completamente. O proprietário deve ser orientado a nunca administrar paracetamol em gatos. Considerando a grande quantidade de gatos atendidos na emergência veterinária com sinais clínicos de intoxicação por paracetamol, tem-se por objetivo apresentar informações sobre essa enfermidade para que os clínicos de pequenos animais possam identifi car o quadro e assim tratá-lo com sucesso.

Paracetamol intoxication in cats occurs due to accidental or iatrogenic exposure, when the owners administers the medication with the intention of treating their pet. Cats are defi cient in terms of biotransformation, so even small doses of the drug can cause toxicity. Among the clinical signs, cyanosis, depression, icterus, edema of face and limbs, tachypnea, dyspnea, anorexia, weakness,vomiting, hypothermia and hematuria can be observed. Fortunately, with aggressive treatment and appropriate supportive care, most animals are able to recover completely. Owners should be advised not to administer acetaminophen in cats. Considering the large number of cats treated in emergency veterinary with clinical signs of acetaminophen toxicity, we have the objective of presenting information about this disease for clinicians of small animals to identify the framework and thus treat it successfully.

Intoxicação por paracetamol em gatos / Acetaminophen toxicity in cats

intoxicação por paracetamol em gatos ocorre por exposição acidental ou de forma iatrogênica, quando um responsável o administra na intenção de tratar seu animal. Os gatos apresentam defi ciência em sua biotransformação e por isso mesmo pequenas doses do fármaco podem provocar sinais de intoxicação. Dentre os sinais clínicos pode-se observar cianose, depressão, icterícia, edema de face e membros, taquipnéia, dispnéia, anorexia, fraqueza, vômito, hipotermia e hematúria. Felizmente, com um tratamento agressivo e cuidado de suporte adequado, a maioria dos animais se recupera completamente. O proprietário deve ser orientado a nunca administrar paracetamol em gatos. Considerando a grande quantidade de gatos atendidos na emergência veterinária com sinais clínicos de intoxicação por paracetamol, tem-se por objetivo apresentar informações sobre essa enfermidade para que os clínicos de pequenos animais possam identifi car o quadro e assim tratá-lo com sucesso.(AU)

Paracetamol intoxication in cats occurs due to accidental or iatrogenic exposure, when the owners administers the medication with the intention of treating their pet. Cats are defi cient in terms of biotransformation, so even small doses of the drug can cause toxicity. Among the clinical signs, cyanosis, depression, icterus, edema of face and limbs, tachypnea, dyspnea, anorexia, weakness,vomiting, hypothermia and hematuria can be observed. Fortunately, with aggressive treatment and appropriate supportive care, most animals are able to recover completely. Owners should be advised not to administer acetaminophen in cats. Considering the large number of cats treated in emergency veterinary with clinical signs of acetaminophen toxicity, we have the objective of presenting information about this disease for clinicians of small animals to identify the framework and thus treat it successfully.(AU)