Introduction. Obesity is one of the most important public health problems in the world. Among obese people, there are those who, apart from excessive body weight, do not exhibit other metabolic dysfunctions, have a lower risk of developing cardiovascular diseases (CVDs), and show lower mortality. According to the theory, they are referred as metabolically healthy obese (MHO), in contrast to metabolically unhealthy obese (MUO). Metabolic disturbances occurring with obesity have been well established to be associated with oxidative stress. Aim. The purpose of this study was to analyse the association between selected anthropometric and biochemical parameters with oxidative stress in MHO, MUO, and normal weight young adults. Material and Methods. Individuals with age between 18 and 36 years with no history of chronic diseases and use of medicaments, with or without obesity, participated in the study. Complete blood counts, biochemical measurements, and parameters of oxidative stress such as total antioxidant capacity (TAC), total oxidative status (TOS), oxidative stress index (OSI), serum concentration of malondialdehyde (MDA), ceruloplasmin, thiol groups and lipid hydroperoxides (LPH), concentration of lipofuscin (LPS) in erythrocytes, and the activity of superoxide dismutase (SOD) were measured. Results. 422 patients who met the inclusion criteria were enrolled in the study. Among the study participants, 208 people (49.29%) were offspring of patients with angiographically confirmed coronary artery disease. Among the participants, 16 patients have been included in the group of metabolically healthy obese (MHO) people and 61 patients in the group of metabolically unhealthy obese (MUO) people and 345 patients had normal body weight. Significant differences between metabolically unhealthy obese and normal weight patients, as well as between women and men, have been found. Conclusions. We showed significant differences in the selected parameters of oxidative stress between metabolically unhealthy obese (MUO) individuals and young volunteers with normal body weight as well as without significant medical history.

The integrated assessment of nutritional status and presence of sarcopenia would help improve clinical outcomes of in-hospital aged patients. We compared three common nutritional screening tools with the new Global Leadership Initiative on Malnutrition (GLIM) diagnostic criteria among hospitalized older patients. To this, 152 older patients were assessed consecutively at hospital admission by the Malnutrition Universal Screening Tool (MUST), the Subjective Global Assessment (SGA), and the Nutritional Risk Screening 2002 (NRS-2002). A 46% prevalence of malnutrition was reported according to GLIM. Sensitivity was 64%, 96% and 47%, and specificity was 82%, 15% and 76% with the MUST, SGA, and NRS-2002, respectively. The concordance with GLIM criteria was 89%, 53% and 62% for the MUST, SGA, and NRS-2002, respectively. All the screening tools had a moderate value to diagnose malnutrition. Moreover, patients at high nutritional risk by MUST were more likely to present with sarcopenia than those at low risk (OR 2.5, CI 1.3-3.6). To conclude, MUST is better than SGA and NRS-2002 at detecting malnutrition in hospitalized older patients diagnosed by the new GLIM criteria. Furthermore, hospitalized older patients at high risk of malnutrition according to MUST are at high risk of presenting with sarcopenia. Nutritional status should be determined by MUST in older patients at hospital admission, followed by both GLIM and the European Working Group on Sarcopenia in Older People (EWGSOP2) assessment.

There are many discrepancies among the results of studies on the genotoxicity of lead. The aim of the study was to explore lead-induced DNA damage, including oxidative damage, in relation to oxidative stress intensity parameters and the antioxidant defense system in human leukocytes. The study population consisted of 100 male workers exposed to lead. According to the blood lead (PbB) levels, they were divided into the following three subgroups: a group with PbB of 20–35 μg/dL (low exposure to lead (LE) group), a group with a PbB of 35–50 µg/dL (medium exposure to lead (ME) group), and a group with a PbB of >50 μg/dL (high exposure to lead (HE) group). The control group consisted of 42 healthy males environmentally exposed to lead (PbB < 10 μg/dL). A comet assay was used to measure the DNA damage in leukocytes. We measured the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) as well as the concentration of malondialdehyde (MDA), and the value of the total antioxidant capacity. The level of PbB was significantly higher in the examined subgroups than in the control group. The percentage of DNA in the tail was significantly higher in the LE, ME, and HE subgroups than in the control group by 10% (p = 0.001), 15% (p < 0.001), and 20% (p < 0.001), respectively. The activity of GR was significantly lower in the LE and ME subgroups than in the control group by 25% (p = 0.007) and 17% (p = 0.028), respectively. The activity of G6PD was significantly lower in the ME subgroup by 25% (p = 0.022), whereas the activity of GST was significantly higher in the HE subgroup by 101% (p = 0.001) than in the control group. Similarly, the activity of SOD was significantly higher in the LE and ME subgroups by 48% (p = 0.026) and 34% (p = 0.002), respectively. The concentration of MDA was significantly higher in the LE, ME, and HE subgroups than in the control group by 43% (p = 0.016), 57% (p < 0.001), and 108% (p < 0.001), respectively. Occupational lead exposure induces DNA damage, including oxidative damage, in human leukocytes. The increase in DNA damage was accompanied by an elevated intensity of oxidative stress.