This manuscript describes the importance of using histological methods to assess the effects of feed on the liver and intestine of fish. Due to the constantly increasing world production of fish and other aquatic organisms, it is necessary to replace fishmeal and fish oil in diets with less expensive raw materials of plant origin. Due to the increased fiber content, increased presence of carbohydrates, antinutritional factors, and inappropriate content of amino acids and new compounds can have negative effects on the digestive system of fish and therefore on fitness, health and production characteristics of cultivated fish. The liver and intestines are the most important organs for the digestion and absorption of nutrients from feed. Therefore, monitoring histological structure of fish liver and intestine is the method of choice in assessing the effects of nutrient mixtures that use raw materials of plant origin. For both of these vital organs the normal histological structure and the most important results obtained by research are discussed. This paper presents a critical review of the histological methods used in research on feed effects. Results related to the negative effects of raw soy-based feed on the occurrence of enteritis in carnivorous fish species are discussed. The results point out that use of modern approach in fish pathology such as improved histochemical, stereological, scoring, and other analytical methods could be a beneficial approach in an accurate assessment of new feed effects on fish

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Abstract. Moderate caloric restriction prolongs lifespan. Changes in oxidative stress and hormesis may be involved in this process. The aim of this study is to examine the effects of different levels of chronic caloric restriction (CR) and acute fasting on stress response and oxidative stress parameters in rat liver and plasma. Forty-two rats were divided into groups: control group, calorie-restricted groups with intake of 80-90%, 60-70%, 40-50%, 20-30% of daily caloric needs and acute fasting group. To determine alanine aminotransferase (ALT), aspartate aminotransferase (AST) and superoxide dismutase (SOD) activity, concentration of corticosterone, nitrites and nitrates (NO x ), malondialdehyde (MDA) and glutathione (GSH), liver samples and blood were collected. Increase in plasma corticosterone concentration and AST and ALT activity was found in severe CR. Ingestion 40-50% daily caloric needs or less increased liver MDA and NO x concentration and decreased SOD activity. Ingestion 60-70% daily caloric needs increased Mn-SOD activity, GSH and NO x . In acute fasting group and group taking 20-30% daily caloric needs, GSH was significantly lower than in control group. Severe CR and acute fasting increase oxidative damage and decrease antioxidative capacity of hepatocytes. Moderate CR increases antioxidative capacity of hepatocytes due to increase in Mn-SOD activity and GSH concentration, which might have a role in anti-aging and hormetic mechanism of CR.

SummaryBackgroundSubclinical hypothyroidism (SCH) is defined as high TSH and normal thyroxine. Data on the effects of early substitution by levothyroxine on psychophysical health in SCH are still not consistent enough to support its introduction.MethodsClinical parameters, biochemical data and quality of life (Short Form 36 questionnaire) were measured before the intervention and 3 months after the euthyroid state had been achieved in SCH patients.ResultsSignificant reduction in body weight (p=0.030), systolic and diastolic blood pressure (p=0.024, p=0.019), homocysteine (p<0.001), leukocytes and neutrophils (p=0.011, p=0.001), INR (p=0.049), K levels (p=0.040, p=0.013), HbA1c (p=0.001), fasting insulin (p<0.001) and insulin resistance measured by HOMA index (p<0.001), lipid parameters (total cholesterol (p<0.001), LDL-cholesterol (p<0.001), triglycerides (p=0.007), apoB (p=0.022), Lp(a) (p<0.001), LDL/HDL (p=0.008), LAP (p=0.04) and apoB/apoA1 ratios (p<0.023)), TSH (p<0.001) and tAbs (p<0.001) was recorded. Frequency of fatty liver (20% to 2.9%, p=0.016), hyperlipidemia (85% to 65.7%, p=0.001) and metabolic syndrome (34.3% to 2.9%, p=0.070) significantly decreased. A statistically significant positive association was found between the average dose of levothyroxine and changes in physical functioning (r=0.391, p=0.020), vitality (r=0.393, p=0.020), mental health (r=0.374, p=0.027) and overall dimensions of mental health (r=0.376, p=0.026). With increasing doses of levothyroxine, the previously listed scores of SF 36 grew (r=0.296, p=0.084).ConclusionsEarly substitution of SCH improved the many clinical and biochemical parameters related to cardiovascular risk. Quality of life was also improved, and correlated only with thyroxine doses suggesting an indirect relationship between the degree of hypothyroidism and quality of life.

We have examined the influence of the nitric oxide (NO)-modified anti-inflammatory drug (S,R)-3-phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) named GIT-27NO or the NOmodified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116. The effects of the drugs on cell viability, apoptosis, proliferation, and metastatic potential were analyzed. The release of NO and oxygen and nitrogen species was also determined. The efficacy of the drugs was evaluated in vivo in BALB/c mice injected with CT26CL25 cells. Both agents suppressed the growth of colon cancer cells in vitro and reduced tumor volume in syngeneic BALB/c mice. However, their mechanisms of action were different because GIT-27NO released larger amounts of nitrite than Saq-NO in cell cultures and its antitumor action depended on the intracellular NO release inside the cells. On the contrary, Saq-NO released barely detectable amounts of NO and its antitumor action was NO-independent. In fact, cotreatment with an NO-peroxynitrite scavenger revealed that GIT-27NO but not Saq-NO acts through peroxynitrite-mediated cell destruction. At the cellular level, GIT-27NO prevalently induced proapoptotic signals followed by caspase-dependent apoptosis. In contrast, Saq-NO blocked cell proliferation, changed the adhesive, migratory, and invasive properties of the cells, and decreased metastatic potential in vivo. In conclusion, differences in NO release and oxidative stress generation between GIT-27NO and Saq-NO resulted in different mechanisms that caused cell death.