Caesalpinia pulcherrima lowered serum carcinoembryonic antigen and antigen 125 in 7,12-Dimethylbenz[a]anthracene-induced Mammary Carcinogenesis in Female Albino Rats.

Aim: This study is aimed at evaluating the anticancer effect of the aqueous extract of Caesalpinia pulcherrima (L.) Sw in 7,12-Dimethlbenz[a]anthracene (DMBA) - induced mammary cancer. Methods: Tumors were induced via a single intraperitoneal injection of DMBA (dissolved in olive oil) at a dose of 80 mg/kg body weight to the test rats and allowed to develop for about four months. They were treated with cyclophosphamide and an aqueous extract of Caesalpinia pulcherrima at doses of 10 and 250 mg/kg body weight, respectively, for 28 days. Serum levels of cancer antigen 125 (CA125), carcinoembryonic antigen (CEA) activity, cyclooxygenase-2 (COX-2), and cytochrome p450 oxidase (cytp450) activity, as well as other diagnostic enzymes, were estimated. Results: The result revealed that DMBA is associated with a significant (p < 0.05) increase in the serum levels of CA125, CEA, COX-2, cytp450, lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) of the rats, thus suggesting tumor-promoting and hepatotoxic effects of DMBA. There was also a significant (p < 0.05) reduction of serum levels of these cancer and liver biomarker enzymes in the groups treated with cyclophosphamide and Caesalpinia pulcherrima compared to the untreated group, thus suggesting anticancer activity of Caesalpinia pulcherrima. The anticancer effect of Caesalpinia pulcherrima was further confirmed by the disappearance of infiltrative fibrous cells and the absence of inflammatory cells from the photomicrographs of the rats treated with Caesalpinia pulcherrima. Conclusion: Our findings show that Caesalpinia pulcherrima possesses anticancer activity, and could protect against mammary cancer.

Tolerance, taxonomic and phylogenetic studies of some bacterial isolates involved in bioremediation of crude oil polluted soil in the southern region of Nigeria.

Indigenous bacteria play vital roles in the bioremediation of crude oil polluted soils. The effectiveness of the bioremediation process depends on the tolerance, characteristics and biodiversity of the bacteria isolates. Bacteria strains were isolated from crude-oil polluted sites in different locations in the southern region of Nigeria namely: Azikoro and Otukpoti (Bayelsa state); Ologbo and Benin (Edo State) and non-polluted soil was collected from Ibadan (Oyo state). Tolerance study was conducted for 96 h s. Isolation and characterization of the most effective isolate from each location was done using cultural, physico-chemical and molecular methods. The tolerance level of the isolates from the different oil-polluted soils and their comparative growth performance on crude oil supplemented media decreases in the order: Azikoro - Ologbo - Otukpoti - Benin. MATS analysis showed that cell surfaces of Azikoro, Ologbo and Otukpoti strains exhibited 58-63 % adhesion to n-hexadecane and are hydrophobic strains while Benin strain possess 38% adhesion to n-hexadecane and are hydrophilic. The cell surfaces of isolates from Azikoro, Ologbo and Otukpoti are highly Lewis-acidic while that from Benin is highly Lewis-basic. Isolates from Benin-3, Ologbo-1, and Otukpoti-1 were shown to be gram positive while that from Azikoro was gram negative. 16S rDNA fingerprinting confirmed the identities of the isolates as follows: Paenalcaligenes suwonesis with accession numbers NR-133804.1 from Azikoro spillage site (93.77%); Lactobacillus nagelii with accession number NR-158108.1 (91.30%) from Benin spillage site; Lactobacillus fermentum with accession number NR-104927.1 (96.70%) from Ologbo and Otukpoti spillage sites. Phylogenetic analysis putatively categorized the isolates from Otukpoti and Ologbo in close association belonging to same homology while Benin isolate is a subgroup. The characteristics and biodiversity of all the isolated bacteria from the regions possibly justifies their involvement in the bioremediation of petroleum hydrocarbons.

Viscum album prevents haematological changes, electrolyte imbalance, changes in liver function enzymes and histological alterations in some selected tissues in cadmium chloride-intoxicated rats.

Background: The use of Viscum album to treat different diseases is popular in the practise of alternative medicine. We investigated the ability of the aqueous extract of V. album to protect against the toxic effects of cadmium. Methods: Thirty rats used for the experiment were treated as follows; Group 1 - no cadmium or extract. Group 2-10 mg/kg body weight of cadmium chloride. Group 3-10 mg/kg body weight of cadmium chloride and 200 mg/kg body weight of aqueous extract of V. album. Group 4-10 mg/kg body weight of cadmium chloride and 400 mg/kg body weight of aqueous extract of V. album. Group 5-10 mg/kg body weight of cadmium chloride with 800 mg/kg body weight of aqueous extract of V. album. Group 6-10 mg/kg body weight of cadmium chloride and atorvastatin (100 mg/kg body weight). Results: Apart from WBC and platelets, other haematological parameters and electrolytes, urea and creatinine levels were not significantly affected by the administration of cadmium chloride along with the aqueous extract of V. album. Treatment with the extract caused significant decreases in the hepatosomatic index, cardiosomatic index, and increase in renosomatic index of the test rats. It also resulted in significant (P < 0.05) decrease in AST level. Histological report also shows that treatment with the extract restored the normal myocardium and vascular architecture of the heart, normal portal and vascular architecture of the liver and normal glomerular and tubular architecture of the kidney, in the cadmium-intoxicated experimental rats. Conclusion: V. album protects against the toxic effects of cadmium chloride.

Evaluation of the haematinic, antioxidant and anti-atherosclerotic potential of Momordica charantia in cholesterol-fed experimental rats.

Background: Momordica charantia is popularly used in folk medicine in the management of hyperlipidemia and atherosclerosis. Purpose: To evaluate the anti-atherosclerotic potential of M. charantia as well as its haematinic and antioxidant potential. Methods: Seventy-two experimental rats were randomly assigned into 9 groups (I-IX) of 8 rats each. Group I (control), was given 1 ml distilled water; II received 250 mg/kg. M. charantia; III received 500 mg/kg M. charantia; IV was administered 100 mg/kg of Atorvastatin only; V was administered 30 mg/kg of cholesterol dissolved in coconut oil; VI was administered with 250 mg/kg of M. charantia plus 30 mg/kg of cholesterol. VII was treated with 500 mg/kg of M. charantia plus 30 mg/kg of cholesterol solution; VIII was administered 30 mg/kg cholesterol solution plus Atorvastatin at a dose of 100 mg/kg; IX was administered 1 ml of coconut oil only. After 60 days of administration, blood and aorta samples were obtained from the rats. The samples were subjected to biochemical, haematological and histological analysis using standard methods. Results: Glutathione peroxidase (GPx), Malondialdehyde (MDA) and Catalase (CAT) activities were significantly higher in the treated groups as compared to the control groups. There were significant increases in the monocyte counts of the groups given low dose (250 mg/kg) of the extract (LDMC), high dose (500 mg/kg) of the extract (HDMC), as well as atorvastatin. The mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH) of the test groups administered were significantly higher than that of the control group. However, only the group administered with cholesterol plus HDMC showed significantly lower mean corpuscular haemoglobin concentration (MCHC) than that of the control group. Histological sections of the aorta show degeneration of the internal elastic lamina in the group fed with the diet only as well as vascular ulceration and stenosis in the aorta and heavy perivascular infiltrates of inflammatory cells. These alterations were however not visible in the groups administered with the extracts, as well as atorvastatin. Conclusion: Our findings show the possible anti-atherosclerotic potential of the extract, which could be compared to that of the standard drug (atorvastatin).

Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na+ channel in the mouse kidney.

Proteolytic activation of the renal epithelial Na+ channel (ENaC) involves cleavage events in its α- and γ-subunits and is thought to mediate Na+ retention in nephrotic syndrome (NS). However, the detection of proteolytically processed ENaC in kidney tissue from nephrotic mice has been elusive so far. We used a refined Western blot technique to reliably discriminate full-length α-ENaC and γ-ENaC and their cleavage products after proteolysis at their proximal and distal cleavage sites (designated from the NH2-terminus), respectively. Proteolytic ENaC activation was investigated in kidneys from mice with experimental NS induced by doxorubicin or inducible podocin deficiency with or without treatment with the serine protease inhibitor aprotinin. Nephrotic mice developed Na+ retention and increased expression of fragments of α-ENaC and γ-ENaC cleaved at both the proximal cleavage site and, more prominently, the distal cleavage site, respectively. Treatment with aprotinin but not with the mineralocorticoid receptor antagonist canrenoate prevented Na+ retention and upregulation of the cleavage products in nephrotic mice. Increased expression of cleavage products of α-ENaC and γ-ENaC was similarly found in healthy mice treated with a low-salt diet, sensitive to mineralocorticoid receptor blockade. In human nephrectomy specimens, γ-ENaC was found in the full-length form and predominantly cleaved at its distal cleavage site. In conclusion, murine experimental NS leads to aprotinin-sensitive proteolytic activation of ENaC at both proximal and, more prominently, distal cleavage sites of its α- and γ-subunit, most likely by urinary serine protease activity or proteasuria.NEW & NOTEWORTHY This study demonstrates that murine experimental nephrotic syndrome leads to aprotinin-sensitive proteolytic activation of the epithelial Na+ channel at both the α- and γ-subunit, most likely by urinary serine protease activity or proteasuria.

Evaluation of the phytochemical content, in vitro antioxidant capacity, biochemical and histological effects of Dennettia tripetala fruits in healthy rats.

We estimated the content of specific phytochemicals and in vitro antioxidant properties of the powder, aqueous, and ethanolic extracts of ripe Dennettia tripetala fruits. We also tested the biochemical and histological effects of these fruit extracts on healthy rats. Aqueous and ethanolic extracts were prepared from the powder of ripe D. tripetala fruits, and standard phytochemical methods were used to evaluate its phytochemical content and antioxidant properties. Eighteen rats were randomized into three groups, one of which served as control, while the second and third groups received the aqueous and ethanolic extracts of D. tripetala fruits, respectively, at a dose of 1,000 mg/kg bw daily for 28 days. Our results show that the powder as well as the aqueous and ethanolic extracts of ripe D. tripetala fruits contains phenols, flavonoids, saponins, tannins, and alkaloids. The plant powder as well as both extracts scavenged DPPH and hydrogen peroxide as well as reduced ferric ions. The extracts of D. tripetala fruits did not alter liver marker enzymes or serum protein profile of the rats. The extracts also did not alter the serum concentration of urea and creatinine and the antioxidant enzyme activity and lipid peroxidation levels in the liver but altered that of the kidney. The extracts altered the serum and liver lipid profile but not to any significant extents. Also, the extracts caused minimal congestion to the centrioles of the liver but were not in any other way toxic to the liver, kidney, or heart of the rats. Our results point to the fact that the fruits of D. tripetala possess phytochemicals with medicinal properties and are well tolerated by rats.

How ageing increases cancer susceptibility: A tale of two opposing yet synergistic views.

It is well known that with increasing age, the risk of acquiring certain age-related diseases - such as diabetes, cancer, cardiovascular disease and neurodegenerative diseases, increases. Several theories have been proposed to explain the reason why ageing leads to higher susceptibility to disease. Over time, many of these theories have been proven wrong. Currently, the two theories holding the interest of researchers in this field are the oxidative damage theory and hyperfunction theory of ageing. The former is an old theory which explains that ageing is as a result of oxidative damage (to macromolecular components of the cell) by reactive oxygen species produced as a normal part of metabolism. The hyperfunction theory is a much newer theory which explains that ageing is as a result of the unnecessary and unwanted continuation of certain metabolic processes at old age. In this review, we discuss the mechanisms which underlie the development of age-related cancer. We also discuss the aforementioned theories of ageing. We conclude by explaining the opposing views of proponents of both theories and provide a new viewpoint by revealing a point of synergy in the two theories.