Ascorbic acid is a low molecular weight antioxidant well known as anti-scorbut acting vitamin C in humans, primates and guinea pigs. This review summarizes basic data about ascorbic acid in its physiological action point of view. It is divided into biochemistry of ascorbic acid synthesis, mechanism of antioxidant action and participation in anabolism, pharmacokinetics and excretion, exogenous ascorbic acid immunomodulatory effect and participation in infectious diseases, impact on irradiation and intoxication pathogenesis, and supplementary demands. The primary intention was to consider ascorbic acid not only as an antioxidant but also as a chemical compound affecting multiple pathways with a potential beneficial impact in many diseases and processes in human body.

Macrophages play an important role in the immune system. They also participate in multiple processes including angiogenesis and triggering of inflammation. The present study summarizes pieces of knowledge on the importance of macrophages in disease, especially the inflammation. Special attention is paid to the cholinergic anti-inflammatory pathway (CAP) associated with the nicotinic acetylcholine receptor (nAChR) and the parasympathetic nervous system. The current pharmacological effectiveness in suppressing the inflammation in general and the septic shock in particular, is limited. CAP was discovered recently and it seems to be a suitable target for the development of new drugs. Moreover, available drugs binding to either nAChR or acetylcholinesterase (AChE) are candidates for either an inhibition or enhancement of CAP. Though the current scientific databases do not include all necessary data on the association of CAP with body functions and the research is quite intensive, the objective of the present review is to introduce the current trends and to critically evaluate CAP and macrophage-associated pathways.

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The case of an HIV-positive man treated for acute toxoplasmosis with no traces of malignancy is reported. A second lymph node extirpation was performed after 5 months, which identified the presence of Hodgkin and Reed-Sternberg (HRS) cells. This case suggests that toxoplasmosis may cause changes in the regulation of surrounding cells and induce neoplastic proliferation.

Oxidative stress is considered predictors of diseases associated with aging (cardiovascular disease, neurodegenerative disease, malignancies, and others) in HIV-negative general population. Antioxidants were investigated in people living with HIV on antiretroviral treatment to determine whether they had an immunosenescent phenotype that might predispose to the development of premature age-related diseases. Clinical studies in this population are controversial. Methods The study was conducted among 213 subjects with HIV, including 172 subjects on antiretro-virals and 41 subjects before the initiation of treatment. The control group consisted of healthy HIV-negative adults. We compared the reduced glutathione and ferric reducing antioxidant power levels in HIV untreated and treated patients and controls. Significant differences were determined by appropriate statistical tests (t-test, Mann-Whitney U test, Kolmogorov-Smirnov test, ANOVA, Kruskal-Wallis test). Relationships between continuous variables were quantified using Spearman's rank correlation coefficient. Results Glutathione levels were significantly lower in the treated group compared with the untreated group and controls (P ˂ 0.001). Differences in total antioxidant levels between groups were not found. Conclusions Significant decrease of antioxidants was found independent of the virologic status of HIV patients on antiretroviral treatment. Persistence of these abnormal parameters may contribute and predispose to the premature development of diseases associated with aging.