Browsing by Author "Areola ED"

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    Enhanced hepatic glycogen synthesis and suppressed adenosine deaminase activity by lithium attenuates hepatic triglyceride accumulation in nicotine-exposed rats
    (2019) Dangana EO; Michael OS; Omolekulo TE; Areola ED; Olatunji LA
    Reduced liver glycogen synthesis might signify increased glucose flux towards fat synthesis and triggers hepatic triglyceride accumulation and dysmetabolism. Adenosine deaminase (ADA) reduces adenosine content which increases glycogenolysis. In the present study, we evaluate the effect of modulating glycogen synthesis and ADA by lithium chloride (LiCl) on nicotine-induced dysmetabolism. Twenty four male Wistar rats (n = 6/group) were allotted into four groups namely; vehicle-treated (po), nicotine-treated (1.0 mg/kg; po), LiCl-treated (5.0 mg/kg; po) and nicotine + LiCl-treated groups. The treatments lasted for 8 weeks. Nicotine exposure resulted in reduced body weight gain, liver weight, visceral adiposity, glycogen content and synthase. Along with increased insulin resistance (IR), fasting plasma glucose, lactate, plasma and hepatic ADA, XO, UA, and triglyceride (TG), total cholesterol (TC), free fatty acid, lipid peroxidation and liver injury markers. However, plasma and hepatic glucose-6-phosphate dehydrogenase-dependent antioxidant defenses were not affected by nicotine exposure. Concurrent treatment with LiCl normalizes all alterations with exception of hepatic TC. This result shows that enhancement of hepatic glycogen synthesis and suppression of ADA/XO/uric acid pathway by lithium can salvage the liver from nicotine-induced TG accumulation.
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    Estrogen-progestin oral contraceptive and nicotine exposure synergistically confers cardio-renoprotection in female Wistar rats
    (2020) Michael OS; Dibia CL; Adeyanju OA; Olaniyi KS; Areola ED; Olatunji LA
    Approximately fifty percent of premenopausal women who smoke cigarettes or on nicotine replacement therapy are also on hormonal contraceptives, especially oral estrogen-progestin. Oral estrogen-progestin therapy has been reported to promote insulin resistance (IR) which causes lipid influx into non-adipose tissue and impairs Na+/K+ -ATPase activity, especially in the heart and kidney. However, the effects of nicotine on excess lipid and altered Na+/K+ -ATPase activity associated with the use of estrogen-progestin therapy have not been fully elucidated. This study therefore aimed at investigating the effect of nicotine on cardiac and renal lipid influx and Na+/K+ -ATPase activity during estrogen-progestin therapy. Twenty-four female Wistar rats grouped into 4 (n = 6/group) received (p.o.) vehicle, nicotine (1.0 mg/kg) with or without estrogen-progestin steroids (1.0 μg ethinyl estradiol and 5.0 μg levonorgestrel) and estrogen-progestin only daily for 6 weeks. Data showed that estrogen-progestin treatment or nicotine exposure caused IR, hyperinsulinemia, increased cardiac and renal uric acid, malondialdehyde, triglyceride, glycogen synthase kinase-3, plasminogen activator inhibitor-1, reduced bilirubin and circulating estradiol. Estrogen-progestin treatment led to decreased cardiac Na+/K+-ATPase activity while nicotine did not alter Na+/K+-ATPase activity but increased plasma and tissue cotinine. Renal Na+/K+-ATPase activity was not altered by the treatments. However, all these alterations were reversed following combined administration of oral estrogen-progestin therapy and nicotine. The present study therefore demonstrates that oral estrogen-progestin therapy and nicotine exposure synergistically prevents IR-linked cardio-renotoxicity with corresponding improvement in cardiac and renal lipid accumulation, oxidative stress, inflammation and Na+/K+-ATPase activity.
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    Regulatory effects of quercetin on testicular histopathology induced by cyanide in Wistar rats
    (2021) Oyewopo AO; Adeleke O; Johnson O; Akingbade A; Olaniyi KS; Areola ED; Tokunbo O
    Several causes of infertility have been identified, and several papers have documented some compounds that cause infertility. One of the compounds reported to be toxic to the reproductive system is cyanide. In the management of infertility, various mechanisms ranging from synthetic drugs, natural products and supplements have been employed. Quercetin is an antioxidant supplement that has been used in the treatment of a variety of ailments. This work is aimed at investigating the role of quercetin in attenuating spermato-toxicity and testicular-histopathology induced by cyanide. Seventy-two (72) male wistar rat (weight 190 g ± 10 g) were divided into nine groups (n = 8) except for groups 4 and 5 with (n = 16). Group 1 (control) received physiological saline while Groups 2 and 3 received 0.5 and 1 mg/kg body weight (bwt) cyanide respectively for 56 days, groups 4 and 5 received 0.5 and 1 mg/kg bwt cyanide respectively for 30 days. At day 30, eight animals were sacrificed from Groups 4 and 5 and the remaining eight (8) rats were subdivided into groups (6 and 7) and were given 20 and 40 mg/kg bwt of quercetin respectively for twenty-six days. Co-administration of cyanide and quercetin at a dose of 0.5 mg/kg cyanide +20 mg/kg quercetin and 1 mg/kg cyanide +40 mg/kg quercetin were given to group 8 and 9 respectively for 56 days. Significant decreases in sperm parameters (count, motile and normal sperm) and increases in malondiadehyde concentration were observed in the cyanide treated groups. Testicular histoarchitecture showed few to no spermatozoa in the lumen of rats treated with cyanide. All these effects were attenuated by quercetin. In conclusion, quercetin regulates testicular histopathology induced by cyanide in Wistar rats. Data from this work suggests potential preventive or therapeutic applications of quercetin for individuals subjected to cyanide environmental pollution.