Environmental and occupational exposure to chromium compounds has become potential aetiologic agent for kidney disease with excessive generation of free radicals, apoptosis, and inflammatory. These pathophysiologic mechanisms of potassium dichromate (K2Cr2O7) have been well correlated with nephrotoxicity and cardiotoxicity. The cardioprotective and nephroprotective effects of Luteolin, a known potent antioxidant were evaluated in this study with 40 healthy rats in four experimental groups: Group A (normal saline), Groups B (30 mg/kg K2Cr2O7), Group C (Luteolin 100 mg/kg and K2Cr2O7 30 mg/kg), and Group D (Luteolin 200 mg/kg and K2Cr2O7 30 mg/kg), respectively. Markers of antioxidant defense system, oxidative stress, blood pressure and micronucleated polychromatic erythrocytes (MnPEs), immunohistochemistry of Kidney, injury molecule (Kim‐1), nuclear factor erythroid 2‐related factor 2 (Nrf2), and cardiac troponin I were determined. Administration of K2Cr2O7 increased blood pressure parameters in systolic, diastolic and mean arterial blood pressures, markers of oxidative stress, and frequency of micronucleated polychromatic erythrocytes, together with reduction in serum nitric oxide level. Renal Kim‐1 and cardiac troponin I expressions were higher, but lower expressions of renal and cardiac Nrf2 were recorded with immunohistochemical analysis. Pre‐treatment with Luteolin restored blood pressure parameters, with concomitant reduction in oxidative stress indicators, augmented antioxidant mechanisms and serum Nitric oxide level, lowered the expressions of Kim‐1, cardiac troponin I and up‐regulated of both cardiac and renal Nrf2, reduced the frequency of micronucleated polychromatic erythrocytes. Taken together, this study therefore demonstrates the cardioprotective, nephro protective and antigenotoxic effects of Luteolin through antioxidantive and radical scavenging mechanisms.

Aim: The opening of mitochondrial permeability transition (mPT) pore is an important event in the execution of mitochondrial-mediated apoptosis. Some bioactive compounds elicit their chemotherapeutic effects against tumor/cancer cells via the induction of mitochondrial-mediated apoptosis. Annona muricata, a medicinal plant, is folklorically used in the treatment of tumors and cancers. This study therefore aimed at investigating the effect of methanol stem bark extract of Annona muricata (MEAM) on apoptosis via mPT pore and estradiol benzoate (EB)-induced proliferative disorder using female Wistar rats. Methodology: Mitochondria were isolated using differential centrifugation. The mPT pore opening, cytochrome c release and mitochondrial ATPase activity were determined spectrophotometrically. The levels of estrogen (E2), luteinizing hormone (LH), follicle stimulating hormone (FSH), malondialdehyde (MDA) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH), were determined using ELISA technique. Histological and histochemical assessments of the uterine sections were carried out using standard methods. Phytochemical constituents of MEAM were determined using Gas Chromatography-Mass Spectroscopy (GC-MS). Results: The in vitro results showed a significant induction of mPT pore opening, release of cytochrome c and enhancement of mitochondrial ATPase (mATPase) activity in a concentration-dependent manner. However, oral administration of MEAM did not induce rat uterine mPT pore opening, neither any significant release of cytochrome c nor enhancement of mATPase activity at the dosages used. Interestingly, MEAM reversed the EB-induced increase in E2, LH and FSH. The MEAM also improved the antioxidant milleu by reducing MDA level and increasing the SOD and GSH-Px activities in the treatment groups. Administration of EB induced endometrial hyperplasia in the model group which was mitigated by MEAM in the treatment group. The GC-MS analysis of MEAM revealed the presence of some important phytochemicals that are pharmacological relevant in cancer treatment. Conclusions: This study suggests that the methanol stem bark extract of Annona muricata contains bioactive compounds that protect against EB-induced uterine proliferative disorder in female Wistar rats.

Diabetes mellitus (DM) is a metabolic disorder leading to high level of morbidity and mortality in human population and it has been identified as the leading cause of death from non-infectious diseases. The use of dexamethasone has been on the increase due to wide array of therapeutic effects it has and the use has mostly been without prescription, since it is a non- prescription drug. Therefore, the potential of dexamethasone to induce DM was studied. Some of the drugs currently used in the treatment of diabetes have their own problematic effects and also expensive, Annona muricata methanolic bark extract(AMMBE) was used in the treatment of dexamethasone-induced diabetes in rats. The research was carried out on albino rats in Federal College of Animal Health and Production Technology, Ibadan and lasted for twenty-eight (28) days. The rats were allotted into four groups (A, B, C and D). Group B, C and D were induced with glucocorticoid (Dexamethasone) (2mgkg-1) daily for seven (7) days intraperitoneally, while group A which was the positive control were given distilled water throughout without induction with glucocorticoid. Group B (the negative control) was induced with glucocorticoid with noAMMBE administration. Group C, was induced and treated with AMMBE at 400 mgkg-1for 14 days. While Group D, was induced with glucocorticoid and were treated with the standard drug (glibenclamide) at 2.5mgkg-1body weight of the rats daily for 14 days. Organ samples of liver, kidney and pancreas were collected for histopathological lesions evaluation. The result showed that dexamethasone induced diabetes after seven (7) days of intraperitoneal administration of 2 mgkg-1 body weights with the glucometer readings in most of the albino rats up to and above 129 mgdL-1. The average blood sugar levels in induced groups (B, C and D) were 132.0±4.05, 129.0±1.41 and130.0±2.93, respectively which were not statistically significant (P>0.05). After administration of AMMBE, the average blood sugar level for group B (126.0±1.41) was significantly different (P<0.05) from C (91.0±1.72) and D (87.0±2.97). Clinical signs of alopecia, dehydration, writhing, paw-licking were observed. There were massive losses of pancreatic cell mass grossly afterinduction with dexamethasone. Histopathological lesions observed ranges from no visible lesion in the control and glibenclamide treated groups to accentuation of hepatocytes in the AMMBE treated rats, and marked vacuolar degeneration of hepatocytes in periportal areas to centrilobular area with Kidney degeneration and multifocal coagulation necrosis of tubular epithelium in group induced with dexamethasone but untreated (group B)Diabetogenic potential of dexamethasone and effect Annona muricata methanolic bark extract degeneration, multifoci coagulation and necrosis. The blood sugar levels post exposure to AMMBE and Glibenclamide showed reduction in the sugar levels. It could be concluded that dexamethasone has the potential of inducing diabetes when its use is prolonged and AMMBE has antidiabetic effect which could be fully explored.

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