Investigation of protective effect of resveratrol and coenzyme Q10 against cyclophosphamide-induced lipid peroxidation, oxidative stress and DNA damage in rats.

It is seen that cyclophosphamide, which is used in treating many diseases, especially cancer, causes toxicity in studies, and its metabolites induce oxidative stress. This study aimed to investigate the protective effects of resveratrol and Coenzyme Q10, known for their antioxidant properties, separately and together, against oxidative stress induced by cyclophosphamide. In this study, 35 Wistar albino male rats were divided into five groups. Groups; Control group, cyclophosphamide (CP) group (CP as 75 mg kg i.p. on day 14), coenzyme Q10 (CoQ10) + CP group (20 mg/kg i.p. CoQ10 + 75 mg kg i.p. CP), resveratrol (Res) + CP group (20 mg/kg i.p. Res + 75 mg/kg i.p. CP), CoQ10 + Res + CP group (20 mg/kg i.p Res + 20 mg/kg i.p CoQ10 and 75 mg/kg i.p.CP). At the end of the experiment, the cholesterol, creatinine and urea levels of the group given CP increased, while a decrease was observed in the groups given Res and CoQ10. Malondialdehyde level was high, glutathione level, superoxide dismutase and catalase activities were decreased in the blood and all tissues (liver, kidney, brain, heart and testis) of the CP given group. DNA damage and histopathological changes were also observed. In contrast, Res and CoQ10, both separately and together, reversed the CP-induced altered level and enzyme activities and ameliorated DNA damage and histopathological changes. In this study, the effects of Res and CoQ10 against CP toxicity were examined both separately and together.

Synergistic toxicity of 2,4-dichlorophenoxyacetic acid and arsenic alters biomarkers in rats.

2,4-dichlorophenoxyacetic acid (2,4-D) and arsenic cause severe and extensive biological toxicity in organisms. However, their interactions and toxic mechanisms in co-exposure remain to be fully elucidated. In this study, 28 four-week-old female rats were divided into four groups and exposed to 100 mg/L arsenic or/and 600 mg/L 2,4-D through drinking water for a period of 28 days. As a result, it was revealed that biochemical indicators (ALT, AST, ALP, blood urea nitrogen, and creatinine) were increased and decreased hormonal parameters (FSH, LH, PG, and E2) in arsenic and 2,4-D and arsenic combination-treated groups. Moreover, increased lipid peroxidation (malondialdehyde level) and decreased antioxidant status (superoxide dismutase and catalase activities) were found in the co-exposure groups compared with the individual-exposure groups. Meanwhile, severe DNA damage was observed in co-exposure groups. Additionally, the levels of apoptotic (Bax, Caspase-3, Caspase-8, Caspase-9, p53, and PARP) and inflammation (NFκB, Cox-2, TNF-α, and TGFßI) indexes in the co-exposure groups were markedly increased, whereas the levels of anti-apoptosis index (Bcl-2) were decreased. It was also observed that co-exposure with 2,4-D and arsenic caused more histopathological changes in tissues. Generally, these results show that co-exposure to 2,4-D and arsenic can seriously cause oxidative stress, DNA damage, apoptosis and inflammation while having toxicological risk for organisms.

The effects of boron on some biochemical parameters: A review.

BACKGROUND: Boron; It is used mainly in glass and ceramics, in the defense industry, in jet and rocket fuel, as a disinfectant, and even in the agricultural sector to increase or prevent vegetation development. Its use in the health field has become more widespread when studies in recent years are reviewed. Although it has been reported that boron has essential biological effects on minerals, some enzymes, and hormones, the mechanism of these biological effects has yet to be fully elucidated. This review aims to bring a new perspective to researchers by combining the results of experimental studies in the literature on the effects of boron on some biochemical parameters. METHODS: Works of literature on boron were brought together using more than one database (WOS, PubMed, Scopus, Google Scholar). The animal, boron type and dose used in the experimental study, and biochemical parameters (glucose, urea, BUN (blood urea nitrogen), uric acid, creatinine, creatine kinase, blood lipid profile, minerals, liver function tests) were systematically compiled. RESULTS: It was observed that the studies mainly focused on glucose and lipid profiles and had a lowering effect on these parameters. From a mineral point of view, the studies are mostly related to the bone matrix. CONCLUSION: Although the mechanism of action of boron on biochemical parameters has not yet been clarified, it would be beneficial to examine its relationship with hormones in more depth. A good understanding and analysis of the effect of boron, which is widely used, on biochemical parameters will be beneficial in taking necessary precautions for human and environmental health.

The effects of boron-supplemented diets on adipogenesis-related gene expressions, anti-inflammatory, and antioxidative response in high-fat fed rats.

The fatty liver syndrome caused by nutritional factors is a common cause of hepatic dysfunction globally. This research was designed to study the shielding effect of boron in rats fed a diet having high fat. Overall, 40 Wistar albino male rats were placed into one control and four treatment groups, that is, each having eight rats. Group I was provided with a standard rat diet while group II was only provided a high-fat diet for 60 days. Groups III, IV, and V were provided with 5, 10, and 20 mg/kg/day boron, respectively, by gastric gavage besides a high-fat diet for 60 days. Malondialdehyde was increased significantly in rats' blood and tissue because of high-fat diets. Glutathione was decreased significantly in blood and tissues because of a high-fat diet. Moreover, the activities of superoxide dismutase (SOD) and catalase (CAT) were decreased in the blood and tissues of the high-fat-fed rats. The genes expression for C-reactive protein, interleukin-1ß, leptin, and tumor necrosis factor-α were increased while gene expression for peroxisome proliferator-activated receptors was decreased in the liver of rats fed with a high-fat diet. Contrariwise, boron supplementation improves antioxidative response in terms of increased SOD and CAT activities, gene expression regulation, and improved anti-inflammatory activities. In a nutshell, boron has dose-dependent shielding antioxidative and tissue regenerative effects in rats.

Synergistic toxicity of ethanol and 2,4-dichlorophenoxyacetic acid enhances oxidant status, DNA damage, inflammation, and apoptosis in rats.

Clarifying the interactions between substances as a result of exposure to multiple xenobiotics and determining the impacts on health are important from the toxicological point of view. Therefore, the aim of the study was to investigate the synergistic toxic effects of ethanol and 2,4-dichlorophenoxyacetic acid (2,4-D) in male albino rats. A total number of 28 Wistar male rats were divided into 4 groups (7/each), and 2,4-D (5 mg/kg) and ethanol (3 g/kg) were administered orally to rats for 60 days, either alone or in combination. Co-administration of ethanol and 2,4-D increased liver functional enzyme levels and lipid peroxidation in blood and tissues while decreased glutathione and antioxidant enzyme activities when compared to individual applications. Furthermore, co-administration of ethanol and 2,4-D caused DNA damage as well as the increase in apoptotic and proinflammatory cytokine gene expressions. Furthermore, histopathological examination of the tissues especially liver and kidney revealed that these two substances induced more serious damage. In conclusion, co-administration of ethanol and 2,4-D resulted in strong toxic effects on tissues (especially liver) with a synergistic interaction and give rise to serious toxicological drawbacks.

Potential protective effect of escin from Aesculus hippocastanum extract against cyclophosphamide-induced oxidative stress on rat tissues.

Cyclophosphamide (CP)-also known as cytophosphan-is an alkylating agent that has many side effects in humans and rats. Rats were divided into 5 different groups to evaluate the protective effect of escin (ES) obtained from the horse-chestnut plant (Aesculus hippocastanum) against acute damage induce by CP. Groups: control group, ethanol group, ES group (100 mg/kg body weight (bw) ES for 14 days by gastric gavage), ES + CP group (100 mg/kg bw ES for 14 days by gastric gavage and 75 mg/kg bw CP i.p. on 14th day), and CP group (75 mg/kg bw CP i.p. on 14th day). After the experiment was completed, blood and tissue samples (liver, kidney, heart, brain, lung, and testis) were taken from the rats under anesthesia. When the CP group was compared with the control group, an increase was observed in the level of Malondialdehyde (MDA) in blood and all tissues except the lung, but when it was given together with escin, there was a decrease except kidney and lung (P < 0.05). Glutathione (GSH) level decreased in the blood and all tissues when CP was given, whereas an increase was observed in the heart, brain, and lung when given with escin (P < 0.05). There was no statistical change in the activities of superoxide dismutase and catalase enzymes in all tissues. ES reduced CP-induced damage in all tissues except the kidney. As a result, it was determined that ES had a protective effect against CP-induced tissue damage in rats due to its antioxidant properties.

Investigation of the effect of boron on thyroid functions and biochemical parameters in hypothyroid induced-rats.

In the study investigating the effects of boron on thyroid hormones and some biochemical parameters in hypothyroid rats, 49 Wistar Albino male rats were divided into seven groups; (Control (C), Hypothyroidism (H), boron groups (B10, and B20), hypothyroid + boron groups (HB10 and HB20), and Treatment (T). Four groups (H, HB10, HB20, and T) were administered 10 mg/kg (B10 and HB10), 20 mg/kg (B20 and HB20) boron for 3 weeks, respectively after hypothyroidism was induced using Propycil® containing propylthiouracil (PTU). Thyroid hormone analyses and biochemical measurements were made from the serum and thyroid gland tissue was examined histopathologically. According to the findings, the fT3 level increased in the B10 group compared to the control group (p < 0.05). While AST, ALT, and ALP activities were found to be higher in the hypothyroid group than in the control group, AST and ALP activities in the HB10 and HB20 groups decreased to values close to the control group. Total cholesterol levels were found to be lower in boron-given groups compared to control and hypothyroid groups (p < 0.05). Sodium iodide symporter (NIS) immunoreactivity was found to be high in hypothyroid rat groups. As a result, it was observed that the increased AST and ALP activities in rats decreased with boron administration. The serum hormone levels measured in the study are not sufficient to understand the effect of boron on the thyroid gland, and it was concluded that further studies at the molecular level are needed to understand the effects of boron on the thyroid gland.

Boron, a Trace Mineral, Alleviates Gentamicin-Induced Nephrotoxicity in Rats.

The present study was considered to assess the protective effects of boron (B) on gentamicin-induced oxidative stress, proinflammatory cytokines, and histopathological changes in rat kidneys. Rats were split into eight equal groups which were as follows: control (fed with low-boron diet); gentamicin group (100 mg/kg, i.p.); B5, B10, and B20 (5, 10, and 20 mg/kg B, i.p.) groups; gentamicin (100 mg/kg, i.p.) plus B5, B10, and B20 (5, 10, and 20 mg/kg B, i.p.) groups. B was given to rats 4 days before the gentamicin treatment and B administration was completed on the 14th day. Gentamicin administration was started on the 4th day and finished on the 12th day. Gentamicin increased malondialdehyde levels, while reduced glutathione levels in the blood and kidney. Furthermore, superoxide dismutase and catalase activities of erythrocyte were decreased. Besides, serum and kidney nitric oxide and 8-dihydroxyguanidine levels were increased by gentamicin. Additionally, serum levels and kidney mRNA expressions of TNF-α, NFκB, IL-1ß, and IFN-γ were found to be the highest in the gentamicin group. Histopathologically, interstitial hemorrhage and tubular necrosis were detected in the kidneys of the gentamicin group. Nonetheless, B administration reversed gentamicin-induced lipid peroxidation, antioxidant status, and inflammation. In conclusion, B has a preventive effect against gentamicin-induced nephrotoxicity and ameliorates kidney tissues of the rat.

Bisphenol-A induced oxidative stress, inflammatory gene expression, and metabolic and histopathological changes in male Wistar albino rats: protective role of boron.

Bisphenol A (BPA) is one of the most produced chemicals in the world and has been widely employed in the food industry. Continuous and widespread exposure to BPA through drinking water and food leads to health concerns for humans. This study evaluated the effects of boron (B) on BPA-mediated oxidative stress in male Wistar albino rats. Rats were equally divided into 5 groups; corn oil was given orally to the control group; 25 mg kg-1 of BPA dissolved in corn oil was given orally to the second group. All other groups received the same dose of BPA and different doses of B (5, 10, and 20 mg kg-1 per day, respectively) orally for 30 days. The administration of BPA significantly decreased glutathione levels and increased malondialdehyde levels in rat tissues. Furthermore, BPA treatment reduced the catalase and superoxide dismutase activities in tissues and erythrocytes. Also, mRNA expression levels of TNF-α, IL-1ß, and IL-6 in the brain, liver, and testes of rats were augmented, whereas IL-10 was decreased with BPA treatment. Besides, BPA treatment adversely altered biochemical parameters and caused damage to the cell integrity of rat tissues. However, B administration reversed BPA-induced alterations in rat tissues in a dose-dependent manner. Furthermore, B exhibited antioxidant and anti-inflammatory effects and regulated metabolic and histopathological alterations in male Wistar albino rats exposed to BPA.

Boron ameliorates arsenic-induced DNA damage, proinflammatory cytokine gene expressions, oxidant/antioxidant status, and biochemical parameters in rats.

Arsenic, an element found in nature, causes hazardous effects on living organisms. Meanwhile, natural compounds exhibit protective effects against hazardous substances. This study evaluated the effects of boron against arsenic-induced genotoxicity and altered biochemical parameters in rats. Thirty-five male Wistar albino rats were equally divided into five groups, and the experimental period lasted 30 days. One group was used as the control, and another group was treated with 100 mg/L arsenic in drinking water. The other groups were orally treated with 5, 10, and 20 mg/kg boron plus arsenic (100 mg/L via drinking water). Arsenic caused changes in biochemical parameters, total oxidant/antioxidant status, and DNA damage in mononuclear leukocytes. Moreover, it increased IFN-γ, IL-1ß, TNF-α, and NFκB mRNA expression levels in rat tissue. However, boron treatment improved arsenic-induced alterations in biochemical parameters and increases in DNA damage and proinflammatory cytokine gene expressions.

The subchronic exposure to malathion, an organophosphate pesticide, causes lipid peroxidation, oxidative stress, and tissue damage in rats: the protective role of resveratrol.

The present study was planned to evaluate the protective role of resveratrol (Res) against subchronic malathion exposure in rats over four weeks. In total, 48 Wistar rats were used and divided equally into six groups. The groups were designed as the control group (received only a rodent diet and tap water), the corn oil group (0.5 ml corn oil by the oral route), and the malathion group (100 mg kg-1 day-1 by the oral route). Other three groups received malathion (100 mg kg-1 day-1) plus Res (5, 10, and 20 mg kg-1 day-1, respectively) by the oral route. Malathion increased malondialdehyde and 8-OHdG levels, whereas it decreased glutathione levels. Also, acetylcholinesterase, superoxide dismutase, and catalase activities were found to be low in the blood, liver, kidney, heart, and brain tissues. Biochemical parameters were not notably changed in all groups. In contrast, Res treatment inverted malathion-induced oxidative stress, lipid peroxidation, and activity of enzymes. Additionally, malathion-induced histopathological changes in the liver, kidney, heart, and brain were ameliorated by Res treatment. These results demonstrate that malathion increases oxidative stress and decreases the antioxidant status while Res has a protective function against malathion toxicity in rats.

The ameliorative effects of boron against acrylamide-induced oxidative stress, inflammatory response, and metabolic changes in rats.

Acrylamide (ACR) is a hazardous substance associated with the accumulation of excessive reactive oxygen species and causes oxidative stress. Presence of ACR in foods leads to public health concerns due to its known neurotoxic, genotoxic, and carcinogenic effects. The present study investigated the ameliorative effects of boron (B) against ACR exposed rats. Forty Wistar albino male rats, fed with low-boron diet, were randomly and equally allocated into 5 groups. The control group was orally treated with physiological saline as placebo, the second group was orally given 15 mg/kg ACR. The other groups were orally treated with 15 mg/kg ACR and B at the levels of 5, 10, and 20 mg/kg/day for 60 days, respectively. ACR-treatment significantly increased malondialdehyde levels whereas decreased glutathione levels in rat tissues. Also, ACR-treatment increased the activities of superoxide dismutase and catalase in erythrocytes and tissues. Meanwhile, mRNA expression levels of NFĸB, IFN-γ, IL-1ß, and TNF-α in liver and brain of rats were increased under ACR treatment. Additionally, ACR caused a significant decrease in the level of high-density lipoprotein, with increase in the levels of low-density lipoprotein, triglyceride, cholesterol, glucose, urea nitrogen, and creatinine. Lastly, B alleviated histopathological alterations induced by ACR in rat tissues.

In vivo assessment of polydatin, a natural polyphenol compound, on arsenic-induced free radical overproduction, gene expression, and genotoxicity.

Arsenic (As) is a well-known contaminant of global groundwater. Its exposure causes several hazardous effects on animals and human via oxidative stress. The present study examined the effect of polydatin (PD) on free radical overproduction in rats exposed to As. Thirty-five male rats randomly allocated into five equal groups. To the control group, physiological saline was given orally and to the second group only 100 mg/L As was given by drinking water for 60 days. The other groups were treated with As (100 mg/L) and PD orally at 50, 100, and 200 mg/kg/day, respectively. Treatment with As enhanced malondialdehyde level but decreased glutathione level in blood, liver, kidney, brain, lung, and heart of rats. Also, As decreased superoxide dismutase and catalase activities of erythrocyte, liver, kidney, brain, lung, and heart in rats. Furthermore, As treatment gave rise to increased DNA damage and gene expressions of interleukin 1 beta (IL-1ß), nuclear factor kappa beta (NFκB), p53, and tumor necrosis factor-α (TNF-α) in the lung, brain, kidney, and liver. However, treatment of PD ameliorated As-exposed lipid peroxidation, antioxidant enzymes activities, DNA damage, gene expressions, and histopathological changes in tissues. In conclusion, PD has a dose-dependent protective effect on lipid peroxidation and antioxidant defense mechanism in rats against As exposure.

Taurine alleviates malathion induced lipid peroxidation, oxidative stress, and proinflammatory cytokine gene expressions in rats.

The present study was considered to evaluate the protective effect of taurine on malathion-induced toxicity in rats. Totally, 48 male rats were divided into 6 equal groups: 0.5ml physiological salt solution was given orally to control rats. 0.5ml corn oil was given orally to rats in corn oil group. Malathion at dose of 27mg/kg (1/50 of LD50) was dissolved in 0.5ml corn oil and given to orally rats in malathion group. The other groups; malathion (27mg/kg) and taurine (dissolved in 0.5ml physiological salt solution) at dose of 50, 100, and 200mg/kg were given orally to rats for 30days, respectively. Malathion treatment decreased acetylcholinesterase levels in serum (30%) and liver (25%) compared to the control group. Malathion resulted in a significant increase in malondialdehyde levels whereas decreased glutathione levels, superoxide dismutase, and catalase activities in rats. Also, IF-γ, IL1-ß, TNF-α, and NFĸB mRNA expression levels were found to be increased 5, 1.7, 2.3, and 2.5 fold in malathion treated rats compared to control, respectively. However, treatment of taurine, in a dose-dependent manner, resulted in a reversal of malathion-induced lipid peroxidation, antioxidant enzyme activities, and mRNA expression levels of proinflammatory cytokines. Moreover, taurine demonstrated preventive action against malathion-induced histopathological changes in rat tissues. In conclusion, taurine exhibited a protective effect in rats against malathion-induced lipid peroxidation, besides it ameliorated antioxidant status, decreased mRNA expression levels of proinflammatory cytokine and repaired rat tissues.

Determination of the regulatory properties of Yucca schidigera extracts on the biochemical parameters and plasma hormone levels associated with obesity

ABSTRACT Yucca schidigera Ortgies, Asparagaceae, is a herbaceous plant. Due to the high saponin content the powdered branches and leaves are used as natural food additive for human and animal. The aim of this study was to investigate the effects of Y. schidigera extracts on plasma leptin, ghrelin, adiponectin, insulin, thyroid hormones and some biochemical parameters in mice fed a high-fat diet. Male Swiss Albino mice were divided into seven equal groups. Group I (negative control group) was given standard diet; Group II was given high-fat diet; Group III was given high-fat diet with carboxymethylcellulose; Groups IV–VII were given hexane, petroleum ether, ethyl acetate, and methanol extracts of Y. schidigera and high-fat diet via gastric gavage for 60 days. High-fat diet significantly increased plasma leptin, insulin, free T3 hormone, glucose, cholesterol, low-density lipoprotein, triacylglyceride, aspartate aminotransferase and alanine aminotransferase levels, and significantly decreased plasma ghrelin, adiponectin and free T4 hormone levels. On the other hand, hormone levels, lipid profile and biochemical parameters were improved by the administration of the PE extract. Y. schidigera extracts could be used as preventive medicine in nutritional disorders via regulating energy metabolism and hormonal functions.

Detection of serum amyloid-A concentration in the calf clinically diagnosed with pneumonia, enteritis and pneumoenteritis / A detecção de amilóide-A concentração sérica na panturrilha com diagnóstico clínico de pneumonia, enterite e pneumoenterites

ABSTRACT: The aim of this study is to determine serum amyloid-A (SAA) concentration in the cases of pneumonia, pneumoenteritis, and enteritis which are frequently encountered in calves in veterinary medicine. Although a great deal of experimental studies has been conducted in this field, studies on naturally infected calves are quite few. Eighty calves at the age of 0-6 months were used in the study and the calves were divided into four groups. Due to the clinical examination, the calves diagnosed with pneumonia (Group P; n=20), with pneumoenteritis (Group PE; n=20) and with enteritis (Group E; n=20) formed the disease group as the healthy ones formed the control (Group C; n=20) group. After the body temperatures of all calves were taken, blood samples were obtained from Jugular vein for haematological and biochemical measurements. As haematological, white blood cell (WBC), red blood cell (RBC), hemoglobin (Hb) and hematocrit (Hct) measurements were performed in Veterinary Hematology Analyzer. Serum amyloid-A (SAA), interleukin 1 (IL-1β), interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) concentration measurements were carried out with ELISA reader by using commercial kits. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin (ALB), total bilirubin (T. Bil), total protein (TP), gamma glutamyltransferase (GGT), blood urea nitrogen (BUN) concentration measurements were conducted in autoanalyzer by using commercial kits. In all disease groups (P, PE, and E) body temperature, haematologic parameters (WBC, RBC, Hb and Hct), serum biochemical parameters (AST, ALT, ALB, T. Bil, TP, GGT and BUN), SAA concentration and serum concentrations of cytokines (IL-1β, IL-6 and TNF-α) were determined to be higher in comparison to the control group (P<0.005). According to these findings, routine measurement of serum SAA concentration in veterinary medicine is considered to be beneficial in determining the severity of the disease, in selecting the proper treatment, in monitoring the applied treatment, and detecting subclinical diseases. In the light of these findings we acknowledge that routine measurements of serum SAA concentration from the moment the calves are diagnosed with pneumonia, enteritis and pneumoenteritis in veterinary medicine until the actual cause is determined (bacteria, virus, parasites, etc.) would avail the clinician to, identify the severity of the disease, select the appropriate treatment and monitor the effectiveness of the treatment.

RESUMO: O objetivo deste estudo é determinar amilóide A (SAA) da concentração sérica nos casos de pneumonia, pneumoenterites e enterite, que são frequentemente encontrados em bezerros em medicina veterinária. Apesar de uma grande quantidade de estudos experimentais terem sido realizados neste campo, os estudos sobre animais com infecção natural são muito poucos. 80 vitelos com a idade de 0-6 meses de idade foram utilizados no estudo e os animais foram divididos em quatro grupos. Devido ao exame clínico, os bezerros diagnosticados com pneumonia (Grupo P; n=20), com pneumoenterites (Grupo PE; n=20) e com enterite (Grupo E; n=20) formaram o grupo de doença, como as saudáveis, ​​formando o grupo controle (Grupo C; n=20). Após as temperaturas corporais de todos os bezerros, foram tomadas amostras de sangue que foram obtidas de veia jugular para medições hematológicas e bioquímicas. Como hematológica, glóbulos brancos (WBC), glóbulos vermelhos (RBC), hemoglobina (Hb) e hematócrito (HCT) foram realizados em Hematologia Veterinária Analyzer. O soro amilóide-A (SAA), a interleucina 1 (IL-1β), interleucina 6 (IL-6), fator de necrose tumoral (TNF-α) medidas de concentração foram efectuadas com um leitor de ELISA, utilizando kits comerciais. Aspartato aminotransferase (AST), alanina aminotransferase (ALT), albumina (ALB), bilirrubina total (T. Bil), proteína total (TP), gama glutamiltransferase (GGT), ureia (BUN) às medições das concentrações foram realizadas em auto-analisador por utilizandos kits comerciais. Em todos os grupos de doenças (P, PE, e E), a temperatura corporal, parâmetros hematológicos (WBC, RBC, Hb e Hct), parâmetros bioquímicos de soro (AST, ALT, ALB, T. Bil, TP, GGT e BUN), a concentração SAA e as concentrações séricas de citocinas (IL-1β, IL-6 e TNF-α) foram determinadas a ser mais elevadas em comparação com o grupo controle (P<0,005). De acordo com estas descobertas, a medição rotineira da concentração de soro SAA em medicina veterinária é considerada benéfica para determinar a gravidade da doença, na selecção de um tratamento adequado, no seguimento do tratamento aplicado e para a detecção de doenças subclínicas. À luz desses resultados, reconhecemos que as medições de rotina da concentração SAA soro do momento em que os bezerros são diagnosticadas com pneumonia, enterite e pneumoenterites em medicina veterinária, até que a causa real seja determinada (bactérias, vírus, parasitas, etc.), seria aproveitar o clínico, a fim de identificar a gravidade da doença, além de seleccionar o tratamento adequado e monitorar a eficácia do tratamento.

The Effects of Boron on Arsenic-Induced Lipid Peroxidation and Antioxidant Status in Male and Female Rats.

The aim of the present study was to investigate the possible protective effects of boron, an antioxidant agent, against arsenic-induced oxidative stress in male and female rats. In total, 42 Wistar albino male and female rats were divided into three equal groups: The animals in the control group were given normal drinking water, the second group was given drinking water with 100 mg/L arsenic, and the third group was orally administered drinking water with 100 mg/kg boron together with arsenic. At the end of the 28-day experiment, arsenic increased lipid peroxidation and damage in the tissues of rats. However, boron treatment reversed this arsenic-induced lipid peroxidation and activities of antioxidant enzymes in rats. Moreover, boron exhibited a protective action against arsenic-induced histopathological changes in the tissues of rats. In conclusion, boron was found to be effective in protecting rats against arsenic-induced lipid peroxidation by enhancing antioxidant defense mechanisms.

Boron attenuates malathion-induced oxidative stress and acetylcholinesterase inhibition in rats.

Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats.

The effects of dietary boron compounds in supplemented diet on hormonal activity and some biochemical parameters in rats.

The aims of this study were to clarify the effects of dietary boric acid or borax, as a boron (B) source, on hormonal status (leptin, insulin, triiodothyronine (T3), and thyroxine) and some biochemical parameter levels as glucose, carnitine, nonesterified fatty acids, and betahydroxybutyric acid in rats. A total of 30 Sprague-Dawley male rats were divided into three equal groups: the animals in the first group (control) were fed with a standard rodent diet containing 6.4 mg B/kg, and the animals in the experimental group were fed with a standard rodent diet added with boric acid and borax (100 mg B/kg) throughout the experimental period of 28 days. The B compounds especially borax decreased leptin, insulin, and glucose levels, whereas increased T3 and carnitine levels in plasma. In addition, body weight of rats was found to be low in the boric acid group at the end of 4 weeks. Consequently, our results demonstrate that B supplementation (100 mg/kg) in diet decreases body weight, leptin, and insulin, whereas increases T3 levels in plasma, so enhances the metabolic activity of rats. Between the B compounds used in this study, it was found that borax had a greater effect on hormonal status than boric acid.

Protective effect of polydatin, a natural precursor of resveratrol, against cisplatin-induced toxicity in rats.

The aim of the present study was to evaluate the possible protective effect of polydatin (PD) on cisplatin (Cis) induced oxidative stress in rats. Totally, thirty male Wistar albino rats were fed standard rodent diet and divided into 5 equal groups: the control group (vehicle treated) was treated with physiological saline for ten days both orally and intraperitoneally (i.p.), the second group was orally treated with physiological saline and 7 mg/kg single i.p. injection of Cis on the seventh day, and third, fourth, and fifth groups were treated orally PD at 25, 50, and 100 mg/kg/day, respectively for 10 days starting seven days before Cis injection and 7 mg/kg single i.p. Cis was injected on the seventh day. Cis resulted in significant increase malondialdehyde levels and decreased glutathione levels. In addition, Cis treatment decreased superoxide dismutase and catalase activities in erythrocyte and tissues. Also, Cis treatment caused to increase DNA damage and affected serum biochemical parameters whereas slightly decreased AchE activity. However, treatment of PD resulted in reversal of Cis-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. In conclusion, PD has protective effect in rats against Cis-induced oxidative stress, enhances antioxidant defence mechanism, and regenerates their tissues.