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The aim of the study was to investigate effects of kaempferol and zinc gluconate administration on haematological, neurobehavioural and oxidative stress changes in Wistar rats, exposed to noise stress. Thirty (30) rats were randomly divided into five groups: Groups I and II were administered with deionised water; Group III, kaempferol; Group IV, zinc gluconate; Group V, kaempferol + zinc gluconate for 36 days. Groups II, III, IV and V were subjected to noise stress of 100 dB dose for 15 days from day 22 to day 36. Behavioural activities were assessed on days 1, 8 and 15 after noise exposure. The effects of the different treatments on body weight change, open-field activities, neuromuscular coordination, motor strength, excitability scores, sensorimotor reflexes and learning and memory were assessed in the rats. Packed cell volume, haemoglobin concentration, total erythrocyte count, erythrocytic indices, platelet count neutrophil/lymphocyte ratio, total and differential leucocyte counts and erythrocyte osmotic fragility (EOF) test were determined using standard methods. The brain was used to evaluate noise stress-induced lipoperoxidative changes, through determination of brain malondialdehyde (MDA) concentration and activities of antioxidant enzymes such as catalase, superoxide dismutase and glutathione peroxidase, using kits. The results of this study showed that noise stress-induced decrease in body weight gain was significantly (P < 0.05) ameliorated in the group treated with kaempferol + zinc (123.70 ± 0.99 g, 133.70 ± 1.59 g) than in the group treated with deionised water + noise (117.70 ± 1.02 g, 125.70 ± 1.20 g). There was a significant and consistent decrease in the EOF of rats treated with kaempferol + zinc. Kaempferol + zinc gluconate significantly (P < 0.05) ameliorated decrease in haemoglobin concentration (from 12.62 ± 0.12 to 14.32 ± 0.11 g/dL), packed cell volume (from 37.85 ± 0.35 to 43.47 ± 0.30 %) and erythrocyte counts (from 6.43 ± 0.04 to 7.20 ± 0.06× 1012/L). Values of mean corpuscular haemoglobin (20.40 ± 0.33 ρg) and mean corpuscular haemoglobin concentration (33.20 ± 0.15%) were significantly (P< 0.05) higher in kaempferol + zinc treated rat compared to the deionized water + noise treated group (18.43 ± 0.34) and (29.65 ± 0.89) respectively. Rats treated with zinc had the highest mean corpuscular volume (61.35 ± 0.67 fL) compared to the deionized water + noise treated group (58.87 ± 0.29). Platelet counts were also significantly higher (P < 0.05) in rats treated with kaempferol + zinc (609.20 ± 6.90 x 106 g/dL) compared to the group treated with noise + deionised water (439.80 ± 7.91 x 106 g/dL). Administration of kaempferol + zinc caused leucocytosis due to neutrophilia and lymphocytosis as well as a significant (P < 0.05) decrease in N:L ratio (0.25 ± 0.01) than in the group treated with deionised water + noise (0.35 ± 0.03). Combination kaempferol + zinc significantly (P < 0.05) enhanced learning (from 2.33 ± 0.33 s to 1.17 ± 0.17) and memory (from 92.17 ± 4.08 s to 106.80 ± 2.14 s). Kaempferol + zinc significantly (P < 0.05) mitigated noise stress induced impairment in neuromuscular coordination neuromuscular coordination (from 45.0 ± 1.43o to 65.06 ± 1.23o), motor strength (from 51.68 ±229 s 78.33 ± 5.69 s), sensory motor reflex (from 2.88 ± 0.16 to 4.83 ± 0.17), and motor coordination on days 1, 8 and 15 (from 10.83 ± 1.40 cm, 11.5 ± 1.18 cm, 10.50 ± 0.923 cm to 5.33 ± 1.45 cm, 4.33 ± 1.41 cm and 4.83 ± 1.35 cm) respectively. Kaempferol + zinc exerted anxiolytic effects, demonstrated in treated rats subjected to open-field test. In addition, combined treatment significantly (P < 0.05) decreased malondialdehyde (MDA) concentration (from 1.10 ± 0.20 nmol/mg to 0.70 ± 0.20 nmol/mg) and enhanced activities of antioxidant enzymes: catalase (from 32.50 ± 2.20 IU/L to 36.90 ± 2.00 IU/L), glutathione peroxidase (from 25.10 ± 1.10 IU/L to 29.40 ± 1.20 IU/L) and superoxide dismutase (from 1.80 ± 0.20 IU/L to 2.20 ± 0.30 IU/L). In conclusion, treatment with kaempferol and zinc singly and in combination ameliorated noise-induced haematological, neurobehavioral and oxidative stress changes in Wistar rats.



1.1 Background of the Study

Noise is derived from the Latin term “nausea” and has been defined as unwanted sound, which is a potential hazard to communication and health (Ismaila and Odusote, 2014). Stress refers to a non-specific response of the body to unpleasant stimuli, threatening homeostasis and the integrity of the organism (Wankhar et al., 2014; Munne-Bosch and Pinto-Marijuan, 2017). It is a state of threatened homeostasis provoked by psychological, physiological and environmental stressors (Zhang et al., 2015). Noise is measured in decibel (dB) units (Ismaila and Odusote, 2014). Wang et al. (2016) reported that noise exposure is a potent stressor as it increases the levels of the stress hormone, corticosterone. Noise pollution, especially in the urban environment, is on the increase (Öhrström et al., 2006; Michaud et al., 2016; WHO, 2016) and ranks among the environmental stressors with the highest public health impact (WHO, 2016). The auditory effects include hearing impairment and permanent hearing loss due to excessive noise exposure. The non-auditory effects include stress-related, physiological and behavioural effects.

Noise stress induces increased reactive oxygen and nitrogen species (ROS and RNS) generation, which are capable of breaking down lipid and protein molecules and damaging DNA, triggering loss of function and cell death (Henderson et al., 2006; Zhang et al., 2015). The ROS also trigger apoptosis by activating proapoptotic mitogen activated protein (MAP) kinase-signaling pathways (Tao et al., 2015). Oxidative destruction has been associated with ROS-induced diseases (Messarah et al., 2011). Antioxidants are molecules that inhibit and scavenge ROS/RNS and convert them to less dangerous molecules (Michael and Peter, 2015).

1.2 Statement of Research Problem

Noise-induced hearing loss has global implications, with 10 million adults and 5.2 million children in the US, and 250 million people world-wide having a noise-induced hearing loss greater than 25 dB; a clinically significant hearing loss (Tao et al., 2015). Additionally, occupational noise accounts for 16% of the disabling hearing loss in adults world-wide, resulting in decreased economic production (Baliatsa et al., 2016). Nocturnal environmental noise also provokes measurable metabolic and endocrine perturbations, including secretion of adrenaline, noradrenaline, cortisol, increased heart rate and arterial blood pressure, and increased motility. While asleep, these biological responses to noise are mostly unnoticed (Basner and Samel, 2004, 2005; Selander et al., 2009). Data confirm that exposure to traffic noise, not specifically at night, is associated with increased incidence of diabetes mellitus (Sorensen et al., 2013), hypertension (Babisch and Kamp, 2009), stroke among the elderly (Sorensen et al., 2011), and mortality from coronary heart disease (Selander et al., 2009; Sorensen et al., 2011; Floud et al., 2013; Baliatsa et al., 2016).

According to WHO (2016), noise causes health damage every day estimated at 4 million dollars. Moreover, psychoneurotic and psychosomatic complaints are also observed due to noise exposures (Martinho et al., 1999). Zheng and Ariizumi (2007) reported that noise exposure prolongor delays healing of surgical wounds, while three days of noise exposure increases immune function, but 28 days of its exposure suppresses it. In addition, oxidative stress increases in rats subjected to 28 days of noise stress, suggesting that oxidative status at least partially accounts for the immune suppression (Cheng et al., 2011). In farm animals, noise directly affects reproductive physiology and energy consumption (Brouček, 2014). Noise may also have indirect effects on population dynamics through changes in habitat use, courtship and mating, reproduction and parental care (Rabin et al., 2003). Pigs exposed to 90 dB prolonged or intermittent noise resulted in decrease in growth (Otten et al., 2004). When poultry is exposed to intermittent loud noise, egg laying and growth rate decreases while mortality increases (Oh et al., 2011). Losses have been reported from mink farms in the form of premature births, insufficient lactation and females kill their offspring in connection with exposure to sonic booms (Algers et al., 1978). In cattle, exposure to a high-intensity noise (105 dB) results in decrease feed consumption (appetite reduction), milk yield, and effectiveness of the milk ejection reflex (Cwynar and Kolacz, 2011).

Noise-induced hearing loss is the greatest cause of sensory disability (WHO, 2016), affecting up to 1 in 6 of the population. It is estimated that approximately 20% of the burden is generated from excessive noise exposure in occupational and leisure settings (Thorne et al., 2008). Sustained exposure to sound pressure levels greater than 85 dB, or sudden exposure to impulse noise leads to irreversible damage to the sensory structures of the cochlea. Once damaged, the mammalian sensory hair cells do not regenerate, and the loss of hearing is permanent (WHO, 2016).

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