CPT (5) SP (500) SP (1000) SP (1500) CPT+ CPT+ CPT+

FIGURE 5.6 Effect of Spirulina (SP) (500, 1000, 1500 mg kg-1, p.o.) on renal (a) lipid peroxidation, (b) reduced glutathione, (c) superoxide dismutase (SOD), and (d) catalase (CAT) in cisplatin (100 mg kg-1, p.o.) treated rats. *p < .05 as compared to the control group (CTRL); < .05 as compared to the CPT group and with one another. (Kuhad et al., 2006.)

in the apoprotein moiety. The authors also proved that the bilin chromophore significantly inhibits the ONOO(-)-mediated single-strand breaks in supercoiled plasmid DNA in a dose-dependent manner with an IC50 value of 2.9 ± 0.6 mM.26,42

Spirulina and Hepatotoxin-Induced Oxidative Damage

There are certain chemicals that are supposed to be hepatotoxic owing to the formation of the free radicals. Carbon tetrachloride (CCl4) and R-(+)-pulegone-induced hepatotoxicity in rats are few examples of these. Vadiraja et al.,43 studied the effect of c-phycocyanin from S. platensis on carbon tetrachloride and R-(+)-pulegone-induced hepatotoxicity in rats. In this study, a single dose (200 mg/kg) of phycocyanin administered intraperitoneally to rats one or 3 h before R-(+)-pulegone (250 mg/kg) or carbon tetrachloride (0.6 mL/kg) challenge, significantly reduced the different oxid-ative stress parameters and resultant hepatotoxicity caused by these chemicals. The hepatoprotective effect of phycocyanin was therefore attributed to the inhibition of reactions involved in the formation of reactive metabolites and possibly to its radical scavenging activity.43 Similar hepatoprotective effect was seen in experiments where rats were fed an oil extract of Spirulina or its defatted fraction. Recently, Bhat and Madayastha28 reported that c-phycocyanin from Spirulina effectively inhibited CCl4-induced lipid peroxidation in rat liver in vivo. Extract from S. fusiformis also provides protection against mercuric chloride-induced hepatic toxicity.40

Spirulina and Neuronal Oxidative Damage

A recent interesting and elaborate study shows that oral administration of c-phycocyanin (100 mg/kg) in rats prevents kainic-acid-induced behavioral and glial reactivity in the rat hippocampus suggesting a corresponding protective effect on neurons. The study showed that phycocyanin reduced experimental status epilepti-cus, suggesting possible therapeutic intervention in the treatment of some forms of epilepsy. According to the authors, kainic acid (KA) triggered excitotoxicities resulted in the production of ROS. It is therefore postulated that the protective effect of phycocyanin in neuronal damage may be due to its free-radical scavenging and antioxidant properties.26,44 An interesting aspect of this study is the finding that oral administration of phycocyanin exerts its effect in the hippocampus, crossing the hem-atoencephalic barrier. According to the authors, these findings and the virtual lack of toxicity of phycocyanin suggest that this phytochemical could be used in the treatment of neurodegenerative diseases such as Alzheimer's and Parkinsonism.44

Phycocyanin (1-3 mg/mL) prevents cell death caused by 24 h potassium and serum withdrawal in rat cerebellar granule cell (CGC) cultures. After 4 h potassium and serum deprivation, phycocyanin inhibited ROS formation measured as 2',7'-dichlorofluorescein fluorescence, showing its scavenging capability.45 Also pretreat-ment of CGC cultures with phycocyanin reduced thymidine incorporation into DNA below control values and reduced dramatically apoptotic bodies as visualized by propidium iodide, indicating inhibition of apoptosis induced by potassium and serum deprivation. Flow cytometry studies indicated that 24 h potassium and serum deprivation acts as a proliferative signal for CGC, which show an increase in S-phase percentage, and cells progressed into the apoptotic pathway. Phycocyanin protected

CGC from apoptosis induced by potassium and serum deprivation. Equivalent results were found when the neuronal damage in the hippocampus was evaluated through changes in peripheral benzodiazepine receptors (microglial marker) and heat shock protein 27 kD expression (astroglial marker).45 Recently, it is also reported that Spirulina-enriched diets enhance striatal dopamine recovery and induce rapid, transient microglia activation after injury of the rat nigrostriatal dopamine system.46 Spirulina-enriched diets had a significant reduction in the volume of infarction in the cerebral cortex and an increase in poststroke locomotor activity as well as it also resulted in decrease expression in caspase enzyme activity.47

At present, the mechanisms by which phycocyanin exerts its neuroprotective effects are not clear. However, growing evidence supports the hypothesis that the phycobiliprotein, acting as an antioxidant, inhibits neuronal death by a mechanism that involves free radical scavenging and therefore phycocyanin may be useful for the treatment of neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's diseases.


Phycocyanin, a water soluble protein of alga, was first reported as a powerful antioxidant by Romay et al., who demonstrated that phycocyanin was able to scavenge hydroxyl and alkoxyl radicals with activity equal to 0.125 mg/mL of dimethyl sulfoxide and 0.038 ^g/mL of trolox, specific scavengers of these radicals respectively. Phycocyanin also inhibited liver microsomal lipid peroxidation. It is interesting to note that oxygen scavenging activity of c-phycocyanin was only 3 times lower than that of superoxide dismutase (SOD).27 Recently, they also reported that phycocyanin inhibited 2,2'-azobis (imidinoprapane) dihydroxychloride (AAPH)-induced erythrocyte haemolysis in the same way as trolox and ascorbic acid, well-known antioxidants. On the basis of IC50values (concentration of the additive that gave the 50% inhibition of peroxidative damage), phycocyanin was found to be 16 times more efficient as an antioxidant than trolox and about 20 times more efficient than ascorbic acid. These findings were supported by a more recent study that showed that the antioxidant activity of phycocyanobilin (a component of phycocyanin) was greater than that of alpha-tocopherol on a molar basis.30 The antioxidant effect of phycocyanobilin was evaluated against oxidation of methyl linoleate in a hydrophobic system or with phosphatidylcholine liposomes. The study also showed that phycocyanin from spray-dried Spirulina had a similar antioxidant activity as phycocyanin from fresh Spirulina. The results suggest that the antioxidant activity of phycocyanin is attributable to phycocy-anobilin, a prosthetic group in phycocyanin, since the apoprotein component may be denatured upon drying. The fact that the dried phycocyanin showed the same level of activity as the intact protein makes the preparation and utilization of phycocyanin commercially feasible.48-50

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