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The Parkinson's-Reversing Breakthrough

Parkinson Disease Treatment

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Norm.

Sign. rev.

Norm. 9

a A minus sign indicates that treatment with Spirulina began before the drag treatment, which was given starting on Day 0 b Norm. = normalized, that is, not significantly different from control levels. c Sign. rev. = significant reversal of drag-induced inhibition. d Antioxidant enzymes were measured in the liver.

e The highest dose appeared to normalize these enzyme activities, but no statistical comparison was performed between controls and animals treated with drags plus Spirulina.

dose exhibited essentially normal SOD and catalase activity and levels of reduced glutathione.

Cyclosporine is an immunosuppressive agent used to prevent rejection of transplanted organs. It is associated with considerable renal toxicity in up to 30% of patients. When rats were given S. platensis at a dose of 500 mg/kg for 3 days before and 14 days concurrently with cyclosporine treatment, drug-induced changes in renal morphology were largely prevented.17 Markers of renal dysfunction were essentially normalized, including plasma urea and creatinine levels and creatinine and lithium clearance. In addition, Spirulina treatment almost completely reversed the cyclosporine-induced rise in the levels of lipid peroxidation not only in the kidney but also in plasma. It also normalized SOD, GPx, and catalase activity in the kidney.

Doxorubicin (DOX) is a potent antitumor agent used for the treatment of a variety of malignancies. It can induce significant and dose-dependent damage to the heart, leading to congestive heart failure. In a recent study, S. platensis was administered twice daily for 3 days before the first injection of DOX and for 7 weeks thereafter, while DOX was injected once a week for 4 weeks.9 Compared to animals given DOX plus saline, mice that had received the alga exhibited markedly fewer and less severe morphological and ultrastructural changes in the heart and this was associated with significantly reduced levels of lipid peroxidation in this tissue. DOX treatment resulted in a decline in plasma antioxidant activity, and this was partially reversed by Spirulina. In addition, the alga completely restored SOD activity, and GPx activity was also similar to that seen in controls.

Pretreatment with S. fusiformis for 5 days before cisplatin, urethane, cyclophosphamide, or mitomycin-C injection significantly decreased drug-induced hepatic lipid peroxidation in a dose-dependent manner.4,5 The highest dose (1000 mg/kg per day) provided complete protection against lipid peroxidation induced by cyclophospham-ide and mitomycin-C, but not by cisplatin or urethane. All of these drugs significantly inhibited the activity of hepatic GPx, SOD, and catalase and decreased the reduced glutathione content of the liver. Spirulina treatment dose dependently reversed this inhibition, though not to the levels seen in untreated controls. It also provided partial protection from the chromosomal damage associated with these drugs.

Similar results have been obtained when Spirulina or phycocyanin was administered to animals treated with chemicals that simulate certain human diseases. Oral pretreatment with S. maxima for 14 days provided some protection from the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, a chemical used as a model of Parkinson's disease.20 This was evidenced by complete prevention of the drug-induced rise in lipid peroxidation in the brain striatum. In addition, phycocyanin partially restored striatal dopamine levels, but this effect was dose-independent.

Kainic acid is a chemical used to model epileptic seizures. Phycocyanin given orally before administration of kainic acid resulted in a significant reduction in tremors and seizures, particularly in the groups that received several doses of phycocyanin over the 24-h period before treatment with kainic acid.21 Neuronal damage was also significantly attenuated by phycocyanin treatment, suggesting that a component of this protein was able to cross the blood-brain barrier. This suggests that the same component may also have participated in the neuroprotective effects in the previously described model of Parkinson's disease.

Phycocyanin has also been investigated in a model of toxic liver injury using either carbon tetrachloride or R-(+)-pulegone as hepatotoxic agents.6,11 When injected intraperitoneally 3 h before treatment with a single dose of carbon tetrachloride, phycocyanin completely inhibited the rise in hepatic lipid peroxidation associated with this chemical.11 This was seen at all doses, which ranged from 50 to 200 mg/kg. A single intraperitoneal dose of phycocyanin 1 or 3 h before injection of either carbon tetrachloride or R-(+)-pulegone completely reversed the drug-induced changes in the activity of all liver enzymes tested.6

In summary, the results of the presented studies clearly show that oral administration of the various species of Spirulina can significantly inhibit lipid peroxidation in the tissue that is the main target of the drug toxicity. Similar effects have been reported for phycocyanin. The findings of these studies also demonstrate that Spirulina and its major biliprotein are able to reverse drug-induced inhibition of the antioxidant enzymes, SOD, catalase, and GPx. From the available data, it cannot be established whether this restoration of endogenous antioxidant enzyme activity is the major anti-oxidative mechanism by which Spirulina and phycocyanin protect from drug-induced oxidative stress and the resulting tissue damage. It seems rather likely that the direct radical scavenging and antioxidant activities of Spirulina and phycocyanin also contribute.

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