About-Daily (Circadian) and About-Weekly (Circaseptan) Patterns of Human Salivary Melatonin

Summary: Chronobiology weekly.

Interestingness: 1

Paper by Manfred Herold, Germaine Cornélissen, Mary Jo Rawson, George S. Katinas, Cheryl Alinder, Chris Bratteli, Denis Gubin, Franz Halberg in the Journal of Anti-Aging Medicine, Volume 3, Issue 3, Spring 2000.


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They analysed the melatonin and cortisol content of the saliva of five people 29-73 years of age for a week. They think there's a weekly cycle in melatonin, peaking on Tuesday. I'm close-minded.
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Abstract follows:

Circadian rhythms in circulating, urinary, salivary, pineal, pituitary and hypothalamic melatonin have been mapped. About weekly (circaseptan) rhythms, mapped previously in several other species, are demonstrated herein for human saliva, in individuals of widely differing ages. Whether or not the now demonstrated decrease with age in the circadian amplitude of human adults is accompanied by an increase in the circaseptan amplitude, as it is the case for blood pressure, remains to be determined.

Serum Schiff Bases Are Elevated in Patients with Dementia

Summary: Schiff bases are more prevalent in demented people's blood, whatever that means. Lipid peroxide levels are lower, whatever that means as well.

Interestingness: 2

Paper by Aleksandra Musial, Tadeusz Pietras And Dariusz Nowak in the Journal of Anti-Aging Medicine, Volume 3, Issue 3, Spring 2000.


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Straight forwards report of testing of four oxidation markers in the blood of 30 old people with clear dementia compared against 18 old people without clear dementia. Conjugated dienes (CnH(2n-2) for values of n, wikipedia tells me) were at about the same concentration in both groups; TBARS (ThioBarbituric Acid Reactive Substances, formed by lipid peroxidation, again, thanks wikipedia) were about 20% higher in demented, but not significant to the 0.05 standard; lipid peroxides were three and a half times higher in the non-demented, and Schiff bases were about 80% higher in the demented.

They are obviously trying to claim higher oxidation levels in the demented. Schiff bases fits their model (I didn't look into how they form). The lower lipid peroxides doesn't, so they come up with reasons. They also find lower lipid peroxides with age in the non-demented group. One possible excuse: lower amounts of poly-unsaturated fatty acids in the brains of older people, supposedly found by someone else.

Anyway, not very interesting, but bonus points for the cool abstract.
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Abstract follows:

Hypothesis

Increased oxidative stress may accompany diseases of the central nervous system either as a perpetrator or merely as the result of tissue damage in the course of neurodegeneration. The brain is especially susceptible to damage mediated by reactive oxygen species because it has a high rate of oxygen consumption and contains large amounts of readily oxidizable substrates, such as polyunsaturated fatty acids. Indices of systemic oxidative stress, including serum lipid-peroxidation products, may be greater in dementia than in normal aging.


Methods

Study groups consisted of 30 patients with dementia and 18 healthy age-matched controls. All patients underwent neuropsychological testing and qualified for the study on the basis of history, physical examination, complementary laboratory tests, and brain computed tomography scan. Serum levels were assessed for the following lipid-peroxidation products: conjugated dienes, lipid peroxides, thiobarbituric acid reactive substances, and Schiff bases.


Results

There were two statistically significant differences in serum levels of lipid-peroxidation products between the study groups. Lipid peroxides were significantly lower (0.34 Å 0.09 U532/mL versus 1.12 Å 0.96 U532/mL, p = 0.000055), while Schiff bases were statistically higher (589.4 Å 267.3 AU/mL versus 329.0 Å 107.5 AU/mL, p = 0.000282) in the subjects with dementia. There were statistically significant correlations between all measured products of lipid peroxidation in the controls and between all products of lipid peroxidation except for Schiff bases in the subjects with dementia. Cognitive impairment did not correlate with levels of lipid-peroxidation products. Age correlated negatively with Mini-Mental State Examination score and lipid peroxides in healthy controls.


Conclusion

More final fluorescent products of lipid peroxidation (Schiff bases) were found in subjects with dementia than in healthy controls, implying that oxidative stress is increased in dementia. Our data suggests a decrease in lipid peroxides during normal aging.

Serum Thiols as a Surrogate Estimate of DNA Repair Correlates to Mammalian Life Span

Summary: Mammalian species with higher thiol fractions in their protein live longer

Interestingness: 2

Paper by Ronald W Pero, Catharina Hoppe and Yezhou Sheng in the Journal of Anti-Aging Medicine, Volume 3, Issue 3, Spring 2000.


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These people grabbed blood samples from mostly one or two specimens of 17 different mammalian species (mouse, rat, wolf, dog, goat, sheep, rabbit, bear, cat, lynx, musk ox, fallow deer, cow, gorilla, chimpanzee, horse and human) and precipitated the proteins in those samples. They found a correlation (r=0.819) between the proportion of thiol in the precipitate and the lifespan of the species (not the specimen, they didn't measure how long the actual specimen they took blood from lived), and a stronger correlation (r=0.841) between the proportion of thiols in the thiol-rich fraction of the proteins and the lifespan of the species.

The plots don't look as good as the r-numbers would indicate because they are heavily influenced by the human specimens since they were many more of them (25 vs 1 or 2 of each of the others), and they are out there way on the right in the lifespan axis (they were assigned a lifespan of 95 years). The graphs don't look horrible either.

Their theoretical explanation confuses me. They are saying that this shows that creatures with higher lifespan have lower oxidation levels. I don't know if they are saying that this is being shown directly, that is oxidation would get rid of the thiol (this assumes that their measuring of the thiols wouldn't count oxidised thiols in them), or that this is being shown indirectly, that is if high lifespan animals didn't have lower oxidisation levels their higher thiol-fractioned proteins would be more affected by oxidation, their enzymes would not work, and so these animals wouldn't have high lifespans. I think they mean the second explanation, but I'm not sure. Backing this second interpretation, is them pointing at the unoxidised thiol-dependence of poly adenosine diphosphate-ribose polymerase (PARP), a DNA-repair enzyme, and from there making other claims about the link between mutation, DNA repair and oxidative stress.
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Abstract follows:

Biologically occurring thiols are a sensitive estimate of the reduction/oxidation balance of cells, being easily and reversibly converted from sulfhydryl to disulfide structures in proteins and amino acids. Thiols are also known to regulate DNA repair, especially via the influence on poly (adenosine diphosphate-ribose) polymerase activity. Here the thiol content of saturated ammonium sulphate-precipitated proteins from sera was correlated to a mammalian life span of 17 species. A close correlation was established between the thiol-rich proteins and the life span of the mammals (r = 0.841, p < 0.001). These data provide a strong scientific connection between mechanisms of DNA repair and oxidative stress leading to DNA damage accumulation and mutation, which may be important to the aging process.