RESUMO
Ozone therapy acts in the body inducing controlled oxidative stress, thereby improving the antioxidant, immune and circulatory responses. However, very little is known about how this therapy affects oxidative stress indicators in dogs. We aimed to assess the clinical, hematological, biochemical and oxidative stress parameters of healthy dogs subjected to ozone therapy and oxygen therapy by rectal insufflation. Ten healthy dogs were allocated into three experimental groups in a cross-over design: control, without intervention; ozone, which received 100 µg of O3/kg through rectal insufflation; and oxygen, which received an ozone-equivalent volume of medicinal O2 through rectal insufflation. Dogs received four applications weekly and were followed up until the seventh week. Ozone therapy significantly increased the weight, mean corpuscular volume and mean platelet volume and decreased total cholesterol of treated dogs. Regarding oxidative stress, ozone therapy reduced total antioxidant capacity by ferric reduction (TAC-FRAP) in D7 compared with baseline and the control, significantly increased total antioxidant capacity by cupric reduction (TAC-CUPRAC) in D42 and D49 compared with the control group, caused an increase in uric acid compared with the oxygen group and decreased lipid peroxidation on D21 compared with the control group. In conclusion, ozone therapy through rectal insufflation causes transient oxidative stress followed by an antioxidant response and discreetly interferes with a few clinical, hematological and biochemical variables in healthy dogs, although variables still remained within the reference ranges for the species, thus proving the safety of the therapy. Furthermore, oxygen therapy causes oxidative stress without inducing a subsequent antioxidant response.
Assuntos
Estudos Cross-Over , Insuflação , Estresse Oxidativo , Ozônio , Reto , Animais , Cães , Ozônio/administração & dosagem , Estresse Oxidativo/efeitos dos fármacos , Reto/efeitos dos fármacos , Masculino , Insuflação/veterinária , Feminino , AntioxidantesRESUMO
Oxidative stress (OS) has been strongly associated with postprandial lipemia (PPL) in humans, and still requires further investigation in dogs. However, since lipemia interferes with spectrophotometric determinations such as those used to assess OS, the present study investigated the effect of PPL on OS parameters of healthy dogs. Twenty dogs had lipemic postprandial samples compared to the average of two non-lipemic moments. Subsequently, PPL was simulated in vitro using a commercial lipid emulsion and twelve pools of non-lipemic serum of these dogs were used to simulate the minimum, median and maximum concentrations of triglycerides obtained during the lipemic state. Serum OS parameters were assessed using the antioxidants uric acid, albumin and total bilirubin; total antioxidant capacity (TAC); total oxidant capacity (TOC); and lipid peroxidation. In vivo PPL caused an increase in albumin, TAC-CUPRAC, TAC-FRAP, uric acid (p < 0.0001), TOC (p = 0.0012) and total bilirubin (p = 0.0245); reduction of TAC-ABTS (p = 0.0008); and did not alter the lipid peroxidation (p = 0.8983). In vitro, levels of albumin increased at the three lipemic concentrations (p < 0.0001), uric acid increased in the median and maximum levels (p < 0.0001), and total bilirubin concentration increased only at the maximum lipemic level (p = 0.0012). All lipemic levels tested increased TAC-ABTS (p = 0.0011) and TAC-FRAP (p < 0.0001). TAC-CUPRAC (p = 0.5002), TOC (p = 0.5938) and lipid peroxidation (p = 0.4235) were not affected by in vitro lipemia. In conclusion, both the in vivo postprandial state and in vitro simulated lipemia affect oxidative stress markers in dogs depending on the oxidative stress marker, and thus the postprandial state and/or lipemic samples should be avoided.