level of the aquatic food chain are prone to higher levels of toxicity present in the
marine or freshwaters [6]. The existence of pharmaceuticals along with their metabolites in water bodies has been reported in many countries [7–9]. Several of these
compounds act as endocrine disrupting chemicals interfering with the normal hormonal balance system [10] by mimicking a natural hormone or blocking the binding
of endogenous hormone to certain receptors [11] and also induce bone marrow,
reproductive and nervous system disorder in living organisms [12, 13].
The major group of pharmaceuticals includes nonsteroidal anti-inflammatory
drugs (NSAIDs), antibiotics, analgesics, lipid regulators, beta-blockers, steroids
and related hormones [14, 15]. NSAIDs act by inhibiting cyclooxygenase (COX)
enzyme which is responsible for the biosynthesis of various active lipid compounds
called prostaglandins [16]. Among the various classes of NSAIDs reported, aspirin,
ibuprofen, naproxen and diclofenac are widely prescribed. NSAIDs are weak
organic acids having a high affinity for lipids and plasma proteins with various
therapeutic potentials.
Aspirin (acetylsalicylic acid, ASA) is one of the most commonly used NSAIDs
worldwide [2, 17]. It is medicated to treat minor pains, cardiovascular thrombosis
[18], arthritis and related musculoskeletal disorders [19]. ASA with the IUPAC
name 2-acetoxy benzoic acid is the NSAID with salicylate chemical group. ASA
is widely used as an analgesic and antipyretic agent as it causes cyclooxygenase
(COX) inhibition on administration [20]. Kerola et al. [21] reported that ASA is
COX-1 specific; COX-1 enzymes are found on the surfaces of platelets and gastric
mucosal cells. The acetyl and the salicylate portions of the ASA molecule produce
analgesic, antipyretic and anti-inflammatory effects when consumed [22]. The activity of cyclooxygenase (COX-1) is hindered by ASA molecule to decrease the
synthesis of precursors of prostaglandins and thromboxanes from arachidonic acid.
Therefore, this helps to regulate the production and release of prostaglandins
preventing the symptoms of inflammatory responses such as swelling, increased
blood vessel dilation, immune response and blood coagulation [23].
The body does not detain the entire dose of drug consumed, as a major portion are
transformed to one or more drug metabolites and are defecated as metabolite
conjugates or parent compounds through urine and faeces [24, 25]. After consumption, acetylsalicylic acid is rapidly hydrolysed into salicyluric acid and glucuronic
acid in the liver and eliminated via urine [26, 27]. The plasma half-life of ASA is
dose-dependent and lengthens as the dose increases [28]. Despite its biodegradable
potential, it is found in river waters [29, 30]. Schulman et al. [31] reported the
presence of ASA in sewage effluents and surface water at maximum loading levels
of 1.5 and ! 3.1 g L
À1 , respectively. The concentrations of ASA reported by Philip
et al. [32] in surface waters of South Indian zone is about 660 ng L
À1 , whereas
samples of pharmaceutical effluents had about 2,270 mg L
À1 of salicylic acid.
ASA exert negative effects on the aquatic ecosystem. Fishes on exposure to
salicylates showed hormonal aberrations and delayed response to an acute stressor
[33, 34]. ASA is teratogenic in rats [35] and also caused maternal toxicity in rabbits
[36]. Exposure of tilapia to ASA induced altered plasma thyroid hormone levels and
cortisol levels [34]. Similarly, the freshwater fishes Cyprinus carpio and Danio
194
S. Siddeswaran et al.
marine or freshwaters [6]. The existence of pharmaceuticals along with their metabolites in water bodies has been reported in many countries [7–9]. Several of these
compounds act as endocrine disrupting chemicals interfering with the normal hormonal balance system [10] by mimicking a natural hormone or blocking the binding
of endogenous hormone to certain receptors [11] and also induce bone marrow,
reproductive and nervous system disorder in living organisms [12, 13].
The major group of pharmaceuticals includes nonsteroidal anti-inflammatory
drugs (NSAIDs), antibiotics, analgesics, lipid regulators, beta-blockers, steroids
and related hormones [14, 15]. NSAIDs act by inhibiting cyclooxygenase (COX)
enzyme which is responsible for the biosynthesis of various active lipid compounds
called prostaglandins [16]. Among the various classes of NSAIDs reported, aspirin,
ibuprofen, naproxen and diclofenac are widely prescribed. NSAIDs are weak
organic acids having a high affinity for lipids and plasma proteins with various
therapeutic potentials.
Aspirin (acetylsalicylic acid, ASA) is one of the most commonly used NSAIDs
worldwide [2, 17]. It is medicated to treat minor pains, cardiovascular thrombosis
[18], arthritis and related musculoskeletal disorders [19]. ASA with the IUPAC
name 2-acetoxy benzoic acid is the NSAID with salicylate chemical group. ASA
is widely used as an analgesic and antipyretic agent as it causes cyclooxygenase
(COX) inhibition on administration [20]. Kerola et al. [21] reported that ASA is
COX-1 specific; COX-1 enzymes are found on the surfaces of platelets and gastric
mucosal cells. The acetyl and the salicylate portions of the ASA molecule produce
analgesic, antipyretic and anti-inflammatory effects when consumed [22]. The activity of cyclooxygenase (COX-1) is hindered by ASA molecule to decrease the
synthesis of precursors of prostaglandins and thromboxanes from arachidonic acid.
Therefore, this helps to regulate the production and release of prostaglandins
preventing the symptoms of inflammatory responses such as swelling, increased
blood vessel dilation, immune response and blood coagulation [23].
The body does not detain the entire dose of drug consumed, as a major portion are
transformed to one or more drug metabolites and are defecated as metabolite
conjugates or parent compounds through urine and faeces [24, 25]. After consumption, acetylsalicylic acid is rapidly hydrolysed into salicyluric acid and glucuronic
acid in the liver and eliminated via urine [26, 27]. The plasma half-life of ASA is
dose-dependent and lengthens as the dose increases [28]. Despite its biodegradable
potential, it is found in river waters [29, 30]. Schulman et al. [31] reported the
presence of ASA in sewage effluents and surface water at maximum loading levels
of 1.5 and ! 3.1 g L
À1 , respectively. The concentrations of ASA reported by Philip
et al. [32] in surface waters of South Indian zone is about 660 ng L
À1 , whereas
samples of pharmaceutical effluents had about 2,270 mg L
À1 of salicylic acid.
ASA exert negative effects on the aquatic ecosystem. Fishes on exposure to
salicylates showed hormonal aberrations and delayed response to an acute stressor
[33, 34]. ASA is teratogenic in rats [35] and also caused maternal toxicity in rabbits
[36]. Exposure of tilapia to ASA induced altered plasma thyroid hormone levels and
cortisol levels [34]. Similarly, the freshwater fishes Cyprinus carpio and Danio
194
S. Siddeswaran et al.