Algae: the game-changers in biohydrogen sector.

Biohydrogen (H2) is an efficient form of renewable energy generated from various biological organisms. Specifically, primitive plants such as algae which are photosynthetic organisms can produce several commercial products, including biofuels due to their simple form, short life span, efficient photosynthetic capacity, and ability to grow in non-potable water sources. But these algae are often neglected and considered waste. Several studies have revealed the importance and role of algal species in generating biofuels, especially biohydrogen. Considerable research has been conducted in order to understand hydrogen production from algal sources. This review emphasizes the photolysis of water-based hydrogen production in algae apart from the metabolites fermentation process. The influence of physico-chemical factors, including oxygen scavengers, nanoparticles, and hydrogenases, was highlighted in this review to enhance H2 production from algal species. Also, several algal species used for hydrogen production are summarized in detail. Overall, this review intends to summarize the developments in hydrogen production from algal species keeping in view of excellent prospects. This knowledge certainly would provide a good opportunity for the industrial production of hydrogen using algal species, which is one of the most concerned areas in the energy sector.

Anti-Inflammatory and Antioxidant Activity of Titanium Dioxide Nanotubes Conjugated with Quercetin.

Inflammation is closely associated with cancer and leads to the formation of various malignancies. Quercetin is a naturally occurring flavonoid, with numerous pharmaceutical activities like anti-oxidant, anti-inflammatory, and anti-tumor effects. Due to its partial solubility in an aqueous solution, its consumption is limited. We recently showed the physicochemical characterization of titanium dioxide nanotubes (TNT) conjugated with quercetin and we found that quercetin conjugated with TNT enhances the anticancer activity in B16F10 cells and induced apoptosis. In the present study, we stimulated the efficiency of quercetin conjugated with titanium dioxide nanotubes and studies their anti-oxidant, anti-inflammatory activity. TNT conjugated with quercetin showed less cytotoxic effect towards RAW264.7 macrophages than quercetin alone. The inflammatory stimulation of RAW264.7 with LPS induced the pro-inflammatory cytokine IL-6 and inducible nitric synthase mRNA which were significantly inhibited by treating with TNT-Qu without causing any toxicity than quercetin and TNT alone. These results suggested that the potential of TNT conjugated with quercetin are better than quercetin and TNT alone and TNT may provide protection against inflammation by down regulating IL-6 and iNOS.

Stat3 Signaling Promotes Survival And Maintenance Of Medullary Thymic Epithelial Cells.

Medullary thymic epithelial cells (mTECs) are essential for establishing central tolerance by expressing a diverse array of self-peptides that delete autoreactive thymocytes and/or divert thymocytes into the regulatory T cell lineage. Activation of the NFκB signaling pathway in mTEC precursors is indispensable for mTEC maturation and proliferation resulting in proper medullary region formation. Here we show that the Stat3-mediated signaling pathway also plays a key role in mTEC development and homeostasis. Expression of a constitutively active Stat3 transgene targeted to the mTEC compartment increases mTEC cellularity and bypasses the requirement for signals from positively selected thymocytes to drive medullary region formation. Conversely, conditional deletion of Stat3 disrupts medullary region architecture and reduces the number of mTECs. Stat3 signaling does not affect mTEC proliferation, but rather promotes survival of immature MHCIIloCD80lo mTEC precursors. In contrast to striking alterations in the mTEC compartment, neither enforced expression nor deletion of Stat3 affects cTEC cellularity or organization. These results demonstrate that in addition to the NFkB pathway, Stat3-mediated signals play an essential role in regulating mTEC cellularity and medullary region homeostasis.

Simultaneous inhibition of T helper 2 and T regulatory cell differentiation by small molecules enhances Bacillus Calmette-Guerin vaccine efficacy against tuberculosis.

Tuberculosis affects nine million individuals and kills almost two million people every year. The only vaccine available, Bacillus Calmette-Guerin (BCG), has been used since its inception in 1921. Although BCG induces host-protective T helper 1 (Th1) cell immune responses, which play a central role in host protection, its efficacy is unsatisfactory, suggesting that additional methods to enhance protective immune responses are needed. Recently we have shown that simultaneous inhibition of Th2 cells and Tregs by using the pharmacological inhibitors suplatast tosylate and D4476, respectively, dramatically enhances Mycobacterium tuberculosis clearance and induces superior Th1 responses. Here we show that treatment with these two drugs during BCG vaccination dramatically improves vaccine efficacy. Furthermore, we demonstrate that these drugs induce a shift in the development of T cell memory, favoring central memory T (Tcm) cell responses over effector memory T (Tem) cell responses. Collectively, our findings provide evidence that simultaneous inhibition of Th2 cells and Tregs during BCG vaccination promotes vaccine efficacy.

Role of thymus in health and disease.

The thymus is a primary lymphoid organ, essential for the development of T-cells that will protect from invading pathogens, immune disorders, and cancer. The thymus decreases in size and cellularity with age referred to as thymus involution or atrophy. This involution causes decreased T-cell development and decreased naive T-cell emigration to the periphery, increased proportion of memory T cells, and a restricted, altered T-cell receptor (TCR) repertoire. The changes in composition and function of the circulating T cell pool as a result of thymic involution led to increased susceptibility to infectious diseases including the recent COVID and a higher risk for autoimmune disorders and cancers. Thymic involution consisting of both structural and functional loss of the thymus has a deleterious effect on T cell development, T cell selection, and tolerance. The mechanisms which act on the structural (cortex and medulla) matrix of the thymus, the gradual accumulation of genetic mutations, and altered gene expressions may lead to immunosenescence as a result of thymus involution. Understanding the molecular mechanisms behind thymic involution is critical for identifying diagnostic biomarkers and targets for treatment help to develop strategies to mitigate thymic involution-associated complications. This review is focused on the consequences of thymic involution in infections, immune disorders, and diseases, identifying potential checkpoints and potential approaches to sustain or restore the function of the thymus particularly in elderly and immune-compromised individuals.

Antioxidant Efficacy of Green-Synthesized Silver Nanoparticles Promotes Wound Healing in Mice.

Developing an efficient and cost-effective wound-healing substance to treat wounds and regenerate skin is desperately needed in the current world. Antioxidant substances are gaining interest in wound healing, and green-synthesized silver nanoparticles have drawn considerable attention in biomedical applications due to their efficient, cost-effective, and non-toxic nature. The present study evaluated in vivo wound healing and antioxidant activities of silver nanoparticles from Azadirachta indica (AAgNPs) and Catharanthus roseus (CAgNPs) leaf extracts in BALB/c mice. We found rapid wound healing, higher collagen deposition, and increased DNA and protein content in AAgNPs- and CAgNPs (1% w/w)-treated wounds than in control and vehicle control wounds. Skin antioxidant enzyme activities (SOD, catalase, GPx, GR) were significantly (p < 0.05) increased after 11 days CAgNPs and AAgNPs treatment. Furthermore, the topical application of CAgNPs and AAgNPs tends to suppress lipid peroxidation in wounded skin samples. Histopathological images evidenced decreased scar width, epithelium restoration, fine collagen deposition, and fewer inflammatory cells in CAgNPs and AAgNPs applied wounds. In vitro, the free radical scavenging activity of CAgNPs and AAgNPs was demonstrated by DPPH and ABTS radical scavenging assays. Our findings suggest that silver nanoparticles prepared from C. roseus and A. indica leaf extracts increased antioxidant status and improved the wound-healing process in mice. Therefore, these silver nanoparticles could be potential natural antioxidants to treat wounds.

Human HMGB1 directly facilitates interactions between nucleotide excision repair proteins on triplex-directed psoralen interstrand crosslinks.

Psoralen is a chemotherapeutic agent that acts by producing DNA interstrand crosslinks (ICLs), which are especially cytotoxic and mutagenic because their complex chemical nature makes them difficult to repair. Proteins from multiple repair pathways, including nucleotide excision repair (NER), are involved in their removal in mammalian cells, but the exact nature of their repair is poorly understood. We have shown previously that HMGB1, a protein involved in chromatin structure, transcriptional regulation, and inflammation, can bind cooperatively to triplex-directed psoralen ICLs with RPA, and that mammalian cells lacking HMGB1 are hypersensitive to psoralen ICLs. However, whether this effect is mediated by a role for HMGB1 in DNA damage recognition is still unknown. Given HMGB1's ability to bind to damaged DNA and its interaction with the RPA protein, we hypothesized that HMGB1 works together with the NER damage recognition proteins to aid in the removal of ICLs. We show here that HMGB1 is capable of binding to triplex-directed psoralen ICLs with the dedicated NER damage recognition complex XPC-RAD23B, as well as XPA-RPA, and that they form a higher-order complex on these lesions. In addition, we demonstrate that HMGB1 interacts with XPC-RAD23B and XPA in the absence of DNA. These findings directly demonstrate interactions between HMGB1 and the NER damage recognition proteins, and suggest that HMGB1 may affect ICL repair by enhancing the interactions between NER damage recognition factors.

Molecular docking analysis of C-phycocyanin with VEGFR2.

C-phycocyanin (C-PC) produced from cyanobacterial species finds application in drug development. Therefore, it is of interest to document the molecular binding features of C-PC with the vascular endothelial growth factor receptor 2 (VEGFR2). C-PC showed H-bond interactions with residues on both sides of the Deusche Forschugsgemein-Schalt (DFG) loop (Asp1046-Phe1047-Gly1048). A hydrophobic association between the activation loop and the DFG residue (Gly1048) helps to inhibit the activity of VEGFR2 kinases. Thus, C-PC is reported as a potential angiogenesis inhibitor for VEGFR2 in combating cancer.

Role of Prostaglandins in Multiple Sclerosis.

Multiple sclerosis (MS) is an autoimmune demyelinating disorder with chronic inflammation in the central nervous system, manifested by both physical and cognitive disability. Neuroinflammation and neurodegeneration are the phenomena that appear in the central nervous system associated with various neurodegenerative disorders, including MS, Alzheimer's diseases, amyotrophic lateral sclerosis and Parkinson's disease. Prostaglandins are one of the major mediators of inflammation that exhibit an important function in enhancing neuroinflammatory and neurodegenerative processes. These mediators would help understand the pathophysiology of MS as the combination of antagonists or agonists of prostaglandins receptors could be beneficial during the treatment of MS. The present review focuses on the role played by different prostaglandins and the enzymes which produced them in the etiopathogenesis of MS.

Green Synthesis of Silver Nanoparticles and Evaluation of Their Antibacterial Activity against Multidrug-Resistant Bacteria and Wound Healing Efficacy Using a Murine Model.

Green nanotechnology has significant applications in various biomedical science fields. In this study, green-synthesized silver nanoparticles, prepared by using Catharanthus roseus and Azadirachta indica extracts, were characterized using UV-Vis spectroscopy, dynamic light scattering, X-ray diffraction, scanning electron microscopy, and transmission electron microscopy. Silver nanoparticles (Ag NPs) synthesized from leaf extracts of C. roseus and A. indica effectively inhibited the growth of multidrug-resistant (MDR) bacteria isolated from patients with septic wound infections. The maximum bacteriolytic activity of the green-synthesized Ag NPs of C. roseus and A. indica against the MDR bacterium K. Pneumoniae was shown by a zone of inhibition of 19 and 16 mm, respectively. C. roseus Ag NPs exhibited more bacteriolytic activity than A. indica Ag NPs in terms of the zone of inhibition. Moreover, these particles were effective in healing wounds in BALB/c mice. Ag NPs of C. roseus and A. indica enhanced wound healing by 94% ± 1% and 87% ± 1%, respectively. Our data suggest that Ag NPs from C. roseus and A. indicia ameliorate excision wounds, and wound healing could be due to their effective antimicrobial activity against MDR bacteria. Hence, these Ag NPs could be potential therapeutic agents for the treatment of wounds.

Potential Therapeutic Applications of C-Phycocyanin.

BACKGROUND: Cancer and other disorders such as inflammation, autoimmune diseases and diabetes are the major health problems observed all over the world. Therefore, identifying a therapeutic target molecule for the treatment of these diseases is urgently needed to benefit public health. C-Phycocyanin (C-PC) is an important light yielding pigment intermittently systematized in the cyanobacterial species along with other algal species. It has numerous applications in the field of biotechnology and drug industry and also possesses antioxidant, anticancer, antiinflammatory, enhanced immune function, including liver and kidney protection properties. The molecular mechanism of action of C-PC for its anticancer activity could be the blockage of cell cycle progression, inducing apoptosis and autophagy in cancer cells. OBJECTIVES: The current review summarizes an update on therapeutic applications of C-PC, its mechanism of action and mainly focuses on the recent development in the field of C-PC as a drug that exhibits beneficial effects against various human diseases including cancer and inflammation. CONCLUSION: The data from various studies suggest the therapeutic applications of C-PC such as anti-cancer activity, anti-inflammation, anti-angiogenic activity and healing capacity of certain autoimmune disorders. Mechanism of action of C-PC for its anticancer activity is the blockage of cell cycle progression, inducing apoptosis and autophagy in cancer cells. The future perspective of C-PC is to identify and define the molecular mechanism of its anti-cancer, anti-inflammatory and antioxidant activities, which would shed light on our knowledge on therapeutic applications of C-PC and may contribute significant benefits to global public health.

Effect of 15-lipoxygenase metabolites, 15-(S)-HPETE and 15-(S)-HETE on chronic myelogenous leukemia cell line K-562: reactive oxygen species (ROS) mediate caspase-dependent apoptosis.

Growth inhibitory effects of 15-lipoxygenase-1 [13-(S)-HPODE and 13-(S)-HODE] and 15-lipoxygenase-2 [15-(S)-HPETE and 15-(S)-HETE] (15-LOX-1 and LOX-2) metabolites and the underlying mechanisms were studied on chronic myeloid leukemia cell line (K-562). The hydroperoxy metabolites, 15-(S)-HPETE and 13-(S)-HPODE rapidly inhibited the growth of K-562 cells by 3h with IC(50) values, 10 and 15microM, respectively. In contrast, the hydroxy metabolite of 15-LOX-2, 15-(S)-HETE, showed 50% inhibition only at 40microM by 6h and 13-(S)-HODE, hydroxy metabolite of 15-LOX-1, showed no significant effect up to 160microM. The cells exposed to 10microM of 15-(S)-HPETE and 40microM of 15-(S)-HETE showed typical apoptotic features like release of cytochrome c, caspase-3 activation and PARP-1 (poly(ADP) ribose polymerase-1) cleavage. A flow cytometry based DCFH-DA analysis and inhibitory studies with DPI, a pharmacological inhibitor of NADPH oxidase, NAC (N-acetyl cysteine) and GSH revealed that NADPH oxidase-mediated generation of ROS is responsible for caspase-3 activation and subsequent induction of apoptosis in the K-562 cell line.

Human XPC-hHR23B interacts with XPA-RPA in the recognition of triplex-directed psoralen DNA interstrand crosslinks.

DNA interstrand crosslinks (ICLs) represent a severe form of damage that blocks DNA metabolic processes and can lead to cell death or carcinogenesis. The repair of DNA ICLs in mammals is not well characterized. We have reported previously that a key protein complex of nucleotide excision repair (NER), XPA-RPA, recognizes DNA ICLs. We now report the use of triplex technology to direct a site-specific psoralen ICL to a target DNA substrate to determine whether the human global genome NER damage recognition complex, XPC-hHR23B, recognizes this lesion. Our results demonstrate that XPC-hHR23B recognizes psoralen ICLs, which have a structure fundamentally different from other lesions that XPC-hHR23B is known to bind, with high affinity and specificity. XPC-hHR23B and XPA-RPA protein complexes were also observed to bind psoralen ICLs simultaneously, demonstrating not only that psoralen ICLs are recognized by XPC-hHR23B alone, but also that XPA-RPA may interact cooperatively with XPC-hHR23B on damaged DNA, forming a multimeric complex. Since XPC-hHR23B and XPA-RPA participate in the recognition and verification of DNA damage, these results support the hypothesis that interplay between components of the global genome repair sub-pathway of NER is critical for the recognition of psoralen DNA ICLs in the mammalian genome.

In vitro and in vivo evaluation of anti-cancer activity: Shape-dependent properties of TiO2 nanostructures.

Cancer is a complex and widespread disease, and it is going to be the first cause of death in the world. Chemotherapy has been used to treat cancer, but it is detrimental to immune cells and known to induce numerous side effects. Therefore it is imperative to develop new drugs for the treatment of cancer without any side effects and toxicity. TiO2 nanomaterials are human safe, cost effective, chemically stable and have numerous biomedical applications. Spherical TiO2 fine particles (TFP), TiO2 nanosquares (TNS) and TiO2 nanotubes (TNT) were developed and evaluated for anti-cancer activity in vitro and in vivo. Our data suggest that these nanostructured materials significantly inhibited proliferation of breast cancer MDAMB 231 cells in in vitro shape dependent manner. In addition, we found that TiO2 nanostructures inhibited the migration and colony formation of breast cancer MDAMB231 cells. More importantly, we found that TNS/TNT/TFP had anti-angiogenic effect in CAM assay and TNT had comparable anti-angiogenic effect with the positive control staurosporine. Additional qRT-PCR data suggest that TiO2 nanostructures induced the upregulation of tumor suppressor genes p53, MDA7, TRAIL and transcription factor STAT3, which suggests the probable mechanism for the anticancer activity of TiO2 nanostructures. Finally, analysis of TEM confirms the dispersion and interaction of nanostructures in the cells. Thus these materials could be potential therapeutic targets for the treatment of cancer.

Immunomodulatory properties of titanium dioxide nanostructural materials.

OBJECTIVES: Although titanium dioxide (TiO2) nanostructural materials have been widely used in Biology and Medicine, very little is known about immunomodulation mechanism of these materials. Objectives of this study are to investigate in vitro immunomodulatory effects of TiO2. Immunosuppressant may lower immune responses and are helpful for the treatment of graft versus host diseases and autoimmune disorders. MATERIALS AND METHODS: In this study, we used H2Ti3O7 titanium dioxide nanotubes (TNT) nanotubes along with commercial TiO2 nanoparticles (TNP) and TiO2 fine particles (TFP). We investigated the in vitro immunomodulatory effects of TNP, TNT, and TFP using mixed lymphocyte reaction (MLR). Suppression was studied by 3-(4, 5-dimethylthiazol-2yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Cytokine profile was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS AND CONCLUSIONS: The results from this study illustrated that the TiO2 nanostructural materials strongly suppressed splenocytes proliferation in MLR. For TNP and TNT, at 50 µg/ml suppression of 20%-25% and 30%-35%, respectively, and for TFP at 100 µg/ml suppression was 25%-30% was observed. Suppression of splenocytes proliferation in the presence of TNP, TNT, and TFP demonstrated that these nanostructural materials probably block T-cell-mediated responses in vitro. Our ELISA results confirmed that significantly lower levels of Th1 type cytokines (interleukin-2, interferon-γ) in the 48 h MLR culture supernatants. Our data suggest that TiO2 nanostructural materials suppress splenocytes proliferation by suppressing Th1 cytokines.

Isolation and in vitro evaluation of bacteriophages against MDR-bacterial isolates from septic wound infections.

Multi-drug resistance has become a major problem for the treatment of pathogenic bacterial infections. The use of bacteriophages is an attractive approach to overcome the problem of drug resistance in several pathogens that cause fatal diseases. Our study aimed to isolate multi drug resistant bacteria from patients with septic wounds and then isolate and apply bacteriophages in vitro as alternative therapeutic agents. Pus samples were aseptically collected from Rajiv Gandhi Institute of Medical Science (RIMS), Kadapa, A.P., and samples were analyzed by gram staining, evaluating morphological characteristics, and biochemical methods. MDR-bacterial strains were collected using the Kirby-Bauer disk diffusion method against a variety of antibiotics. Bacteriophages were collected and tested in vitro for lytic activity against MDR-bacterial isolates. Analysis of the pus swab samples revealed that the most of the isolates detected had Pseudomonas aeruginosa as the predominant bacterium, followed by Staphylococcus aureus, Klebsiella pneumoniae and Escherichia coli. Our results suggested that gram-negative bacteria were more predominant than gram-positive bacteria in septic wounds; most of these isolates were resistant to ampicillin, amoxicillin, penicillin, vancomycin and tetracycline. All the gram-positive isolates (100%) were multi-drug resistant, whereas 86% of the gram-negative isolates had a drug resistant nature. Further bacteriophages isolated from sewage demonstrated perfect lytic activity against the multi-drug resistant bacteria causing septic wounds. In vitro analysis of the isolated bacteriophages demonstrated perfect lysis against the corresponding MDR-bacteria, and these isolated phages may be promising as a first choice for prophylaxis against wound sepsis, Moreover, phage therapy does not enhance multi-drug resistance in bacteria and could work simultaneously on a wide variety of MDR-bacteria when used in a bacteriophage cocktail. Hence, our results suggest that these bacteriophages could be potential therapeutic options for treating septic wounds caused by P. aeruginosa, S. aureus, K. pneumoniae and E. coli.

Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats.

Microbial infections, localized as well as systemic, are known to cause transitive or permanent male infertility. However, the mechanisms of infection-induced infertility are largely unknown. Earlier reports showed that steroidogenesis and spermatogenesis are affected during bacterial lipopolysaccharide (LPS)-induced acute inflammation. The present study used an LPS rat model to investigate the role of oxidative stress in spermatogenesis. Intraperitoneal administration of bacterial LPS (5mg/kg body weight) to adult male albino rats elevated testicular malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE), and decreased the activities of testicular antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. The GSH/GSSG ratio also decreased significantly. Time series analysis revealed transitory oxidative stress and expression of inflammatory mediators such as interleukin-1beta (IL-1beta), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) from 3h to 12h after LPS. Testicular expression of steroidogenic acute regulatory (StAR) protein decreased to 24h, in correlation with damage to spermatogenesis. These data are consistent with oxidative stress as a major causal factor in altered steroidogenesis, spermatogenesis, and perhaps male infertility during endotoxin-induced acute inflammation.

Repair of genome destabilizing lesions.

Living organisms are constantly exposed to detrimental agents both from the environment (e.g. ionizing radiation, ultraviolet light, natural and synthetic chemicals) and from endogenous metabolic processes (e.g. oxidative and hydrolytic reactions), resulting in modifications of proteins, lipids and DNA. Proteins and lipids are degraded and resynthesized, but the DNA is replicated only during cell division, when DNA damage may result in mutation fixation. Thus the DNA damage generated has the potential to lead to carcinogenesis, cell death, or other genetic disorders in the absence of efficient error-free repair. Because modifications in DNA sequence or structure may be incompatible with its essential role in preservation and transmission of genetic information from generation to generation, exquisitely sensitive DNA repair pathways have evolved to maintain genomic stability and cell viability. This review focuses on the repair and processing of genome destabilizing lesions and helical distortions that differ significantly from the canonical B-form DNA in mammalian cells. In particular, we discuss the introduction and processing of site-specific lesions in mammalian cells with an emphasis on psoralen interstrand crosslinks.

Molecular docking and simulation of Curcumin with Geranylgeranyl Transferase1 (GGTase1) and Farnesyl Transferase (FTase).

Protein prenylation is a posttranslational modification that is indispensable for translocation of membrane GTPases like Ras, Rho, Ras etc. Proteins of Ras family undergo farnesylation by FTase while Rho family goes through geranylgeranylation by GGTase1. There is only an infinitesimal difference in signal recognition between FTase and GGTase1. FTase inhibitors mostly end up selecting the cells with mutated Ras proteins that have acquired affinity towards GGTase1 in cancer microcosms. Therefore, it is of interest to identify GGTase1 and FTase dual inhibitors using the docking tool AutoDock Vina. Docking data show that curcumin (from turmeric) has higher binding affinity to GGTase1 than that of established peptidomimetic GGTase1 inhibitors (GGTI) such as GGTI-297, GGTI-298, CHEMBL525185. Curcumin also interacts with FTase with binding energy comparable to co-crystalized compound 2-[3-(3-ethyl-1-methyl-2-oxo-azepan-3-yl)-phenoxy]-4-[1-amino-1-(1-methyl-1h-imidizol-5-yl)-ethyl]-benzonitrile (BNE). The docked complex was further simulated for 10 ns using molecular dynamics simulation for stability. Thus, the molecular basis for curcumin binding to GGTase1 and FTase is reported.

Molecular mechanisms in C-Phycocyanin induced apoptosis in human chronic myeloid leukemia cell line-K562.

C-Phycocyanin (C-PC), the major light harvesting biliprotein from Spirulina platensis is of greater importance because of its various biological and pharmacological properties. It is a water soluble, non-toxic fluorescent protein pigment with potent anti-oxidant, anti-inflammatory and anti-cancer properties. In the present study the effect of highly purified C-PC was tested on growth and multiplication of human chronic myeloid leukemia cell line (K562). The results indicate significant decrease (49%) in the proliferation of K562 cells treated with 50 microM C-PC up to 48 h. Further studies involving fluorescence and electron microscope revealed characteristic apoptotic features like cell shrinkage, membrane blebbing and nuclear condensation. Agarose electrophoresis of genomic DNA of cells treated with C-PC showed fragmentation pattern typical for apoptotic cells. Flow cytometric analysis of cells treated with 25 and 50 microM C-PC for 48 h showed 14.11 and 20.93% cells in sub-G0/G1 phase, respectively. C-PC treatment of K562 cells also resulted in release of cytochrome c into the cytosol and poly(ADP) ribose polymerase (PARP) cleavage. These studies also showed down regulation of anti-apoptotic Bcl-2 but without any changes in pro-apoptotic Bax and thereby tilting the Bcl-2/Bax ratio towards apoptosis. These effects of C-PC appear to be mediated through entry of C-PC into the cytosol by an unknown mechanism. The present study thus demonstrates that C-PC induces apoptosis in K562 cells by cytochrome c release from mitochondria into the cytosol, PARP cleavage and down regulation of Bcl-2.