Autophagy upregulation and loss of NF-kappaB in oxidative stress-related immunodeficient SAMP8 mice.

Aged spleens from senescence-accelerated prone mice 8 (SAMP8) and senescence-accelerated resistant mice 1 (SAMR1) were examined to determine whether sex or melatonin had an effect on oxidative stress-related immune impairments. We observed that the immunosenescence of SAMP8 mice was associated with a redox imbalance, leading to an age-related increase in oxidative damage, resulting from a decrease in antioxidant defense and protease activity. Moreover, increased apoptotic cell death, a decrease in proliferative activity and the loss of NF-kappaB activation were also related to the immunodeficiency seen in SAMP8 compared to SAMR1 mice.

Sexual dimorphism of autophagy in Syrian hamster Harderian gland culminates in a holocrine secretion in female glands.

The Syrian hamster Harderian gland (HG) has a large porphyrin metabolism with a sexual dimorphism, showing male HGs much lower porphyrin concentrations than female glands. Damage derived from this production of porphyrins, displayed by reactive oxygen species, forces the gland to develop morphological changes that must have a physiological significance. Thus, oxidative stress is present in two states: mild oxidative stress in male HGs and extreme oxidative stress in female HGs.

Melatonin alters cell death processes in response to age-related oxidative stress in the brain of senescence-accelerated mice.

We studied the effect of age and melatonin on cell death processes in brain aging. Senescence-accelerated prone mice 8 (SAMP8) and senescence-accelerated resistant mice (SAMR1) at 5 and 10 months of age were used as models of the study. Melatonin (10 mg/kg) or its vehicle (ethanol at 0.

Sexual autophagic differences in the androgen-dependent flank organ of Syrian hamsters.

The flank organ of the Syrian hamster shows a biodynamic response to androgenic stimulation and is, therefore, a suitable model for the study of androgenic effects on hair and sebaceous glands. This organ is susceptible to programmed cell death (PCD), a prominent feature associated with sexual organ adjustment. In the present report, the type of PCD (apoptosis or autophagy) exhibited by this organ was evaluated.

Favorable effects of a prolonged treatment with melatonin on the level of oxidative damage and neurodegeneration in senescence-accelerated mice.

Senescence-accelerated mice (SAMP8) and senescence-accelerated resistant mice (SAMR1) were studied at 5 and 10 months of age, respectively. In the animals, neurodegenerative processes and how they were influenced by melatonin were examined. Melatonin (10 mg/kg) or vehicle (ethanol at 0.

Oxidative damage in the livers of senescence-accelerated mice: a gender-related response.

The prevalence of liver diseases emphasizes the need of animal models to research on the mechanism of disease pathogenesis. Furthermore, most of the liver pathologies have the oxidative stress as an important component. The senescence-accelerated mouse strain SAMP8 was proposed as a valuable animal model for the study of liver diseases.

Antioxidant activity in Spalax ehrenbergi: a possible adaptation to underground stress.

The blind subterranean mole rat Spalax ehrenbergi superspecies has evolved adaptive strategies to cope with underground stress. Hypoxia is known to stimulate reactive oxygen species generation; however, mechanisms by which Spalax counteracts oxidative damage have not been investigated before. We studied in Spalax the oxidative status of the Harderian gland (HG), an organ which is particularly vulnerable to oxidative stress in many rodents.

Survival mechanisms in a physiological oxidative stress model.

The Syrian hamster Harderian gland has as the remarkable feature of an extraordinary rate of porphyrin production, even higher than the liver. The low activity of the last enzyme of the route gives rise to the accumulation of the uncomplex porphyrins in the female glands. Moreover, due to the localization of the Harderian gland, porphyrins exposed to light produce reactive oxygen species and, thus, the gland presents a physiological oxidative stress, with a great number of sings of degeneration, but without compromising the gland integrity.

Melatonin neutralizes neurotoxicity induced by quinolinic acid in brain tissue culture.

Quinolinic acid is a well-known excitotoxin that induces oxidative stress and damage. In the present study, oxidative damage to biomolecules was followed by measuring lipid peroxidation and protein carbonyl formation in rat brain tissue culture over a period of 24 hr of exposure to this prooxidant agent at a concentration of 0.5 mm.

Coexpression of MT1 and RORalpha1 melatonin receptors in the Syrian hamster Harderian gland.

Melatonin acts through several specific receptors, including membrane receptors (MT(1) and MT(2)) and members of the RZR/ROR nuclear receptors family, which have been identified in a large variety of mammalian and nonmammalian cells types. Both membrane and nuclear melatonin receptors have been partially characterized in Harderian gland of the Syrian hamster. Nevertheless, the identities of these receptors were unknown until this study, where the coexistence of MT(1) and RORalpha(1) in this gland was determined by nested RT-PCR followed by amplicon sequencing and Western-blot.

Specific binding of melatonin to purified cell nuclei from mammary gland of swiss mice: day-night variations and effect of continuous light.

Melatonin binding sites were characterized in the nuclei of mouse mammary glands. The specific binding of 2-125I-iodomelatonin by homogenates of purified mammary gland cell nuclei was found to be rapid, reversible and saturable. Binding of 125I-melatonin exhibited day-night variations with the highest binding affinity observed during the dark period and the lowest affinity at midday.

Characterization of melatonin high-affinity binding sites in purified cell nuclei of the hamster (Mesocricetus auratus) harderian gland.

In the present paper, binding of melatonin to purified cell nuclei from harderian glands of male and female hamsters was assessed. Binding of 125I-melatonin to cell nuclei fulfills the criteria for binding to a receptor site. Binding kinetics exhibit properties such as dependence on time and temperature as well as reversibility, saturability, high affinity and specificity.

Effects of continuous light exposure on antioxidant enzymes, porphyric enzymes and cellular damage in the Harderian gland of the Syrian hamster.

The Syrian hamster Harderian gland (HG), an organ present in the male two secretory cell types (type-I and type-II cells), is physiologically exposed to high oxidative stress because of high concentrations of porphyrins and their precursor, 5-aminolevulinic acid. Because of its juxtaorbital location, the HG is accessible to light, and subject to phototoxic effects of these substances. After having previously demonstrated circadian rhythms in antioxidant enzymes, porphyric enzymes and oxidative damage of proteins and lipids, as well as influences of melatonin on these parameters, we have now studied the effects of continuous light (LL), which suppresses melatonin secretion by the pineal gland.

Effects of delta-aminolevulinic acid and melatonin in the harderian gland of female Syrian hamsters.

Effects of delta-aminolevulinic acid (ALA) and melatonin were investigated in the female Syrian hamster Harderian gland. This is an organ physiologically exposed to strong oxidative stress due to the highest porphyrinogenic rates known in nature. Enzyme activities of porphyrin biosynthesis and of antioxidative protection, oxidative protein modification, and histological integrity were studied.

Melatonin protects against delta-aminolevulinic acid-induced oxidative damage in male Syrian hamster Harderian glands.

Effects of the prooxidant delta-aminolevulinic acid (ALA) and the antioxidant melatonin (MEL) were investigated in the male Syrian hamster Harderian gland (HG). Rodent Harderian glands are highly porphyrogenic organs, which may be used as model systems for studying damage by delta-aminolevulinic acid and its metabolites, as occurring in porphyrias. Chronic administration of delta-aminolevulinic acid (2 weeks) markedly decreased activities of the porphyrogenic enzymes delta-aminolevulinate synthase (ALA-S) and delta-aminolevulinate dehydratase (ALA-D) and of the antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR) and catalase (CAT), whereas porphobilinogen deaminase (PBG-D) remained unaffected.