a-collection-of-research-articles-on-the-medical-potential-of-cow-urine
a-collection-of-research-articles-on-the-medical-potential-of-cow-urine a-collection-of-research-articles-on-the-medical-potential-of-cow-urine
1972 Mol Biol Rep (2014) 41:1967–1976 17.08, and 11.95 % respectively, in the levels
Mol Biol Rep (2014) 41:1967–1976 1973 combination
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Mol Biol Rep (2014) 41:1967–1976 1973<br />
combinati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> antioxidants and <strong>cow</strong> <strong>urine</strong> (U?A?L<br />
group) and minimum in <strong>the</strong> <strong>on</strong>ly <strong>cow</strong> <strong>urine</strong> (U?L) group.<br />
The reducti<strong>on</strong> in <strong>the</strong> activity <str<strong>on</strong>g>of</str<strong>on</strong>g> SOD, CAT enzymes<br />
may result in a number <str<strong>on</strong>g>of</str<strong>on</strong>g> deleterious effects due to <strong>the</strong><br />
accumulati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> superoxide ani<strong>on</strong> and hydrogen peroxide<br />
[58]. The eliminati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> H 2 O 2 is ei<strong>the</strong>r effected by CAT or<br />
GPx [69].<br />
The level <str<strong>on</strong>g>of</str<strong>on</strong>g> GPx in <strong>the</strong> exposed group were lowered<br />
which is in accordance with <strong>the</strong> earlier studies where lindane<br />
caused a similar decrease in <strong>the</strong> levels <str<strong>on</strong>g>of</str<strong>on</strong>g> GPx in<br />
various tissues [42, 48]. Renal GPx levels were found to be<br />
decreased due to chlorpryfos-ethyl [46], aflatoxin [61],<br />
acetaminophen [27], cisplatin [4] and CCl 4 [7] toxicity.<br />
The decreased levels can be attributed to ei<strong>the</strong>r increased<br />
H 2 O 2 generati<strong>on</strong> or decreased GSH c<strong>on</strong>centrati<strong>on</strong> because<br />
GSH is <strong>on</strong>e <str<strong>on</strong>g>of</str<strong>on</strong>g> <strong>the</strong> substrates for GPx [57]. A decreased<br />
GSH c<strong>on</strong>centrati<strong>on</strong> was observed in <strong>the</strong> present study.<br />
Decreased activity <str<strong>on</strong>g>of</str<strong>on</strong>g> GPx may also result from radical<br />
induced inactivati<strong>on</strong> and glycati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> <strong>the</strong> enzymes [26].<br />
Because <str<strong>on</strong>g>of</str<strong>on</strong>g> <strong>the</strong> decreased GPx activity <strong>the</strong> accumulati<strong>on</strong><br />
<str<strong>on</strong>g>of</str<strong>on</strong>g> H 2 O 2 may cause inhibiti<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> SOD activity [10]. During<br />
oxidative stress, inactivati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> GPx may occur, and <strong>on</strong> <strong>the</strong><br />
o<strong>the</strong>r hand superoxide ani<strong>on</strong> (O 2 •- ) itself can inhibit peroxidase<br />
functi<strong>on</strong> [12]. So GPx must be c<strong>on</strong>sidered to be<br />
complementary to SOD [43].<br />
The pretreatment with vitamin C, E, lipoic acid and <strong>cow</strong><br />
<strong>urine</strong> in groups A?L, U?L and U?A?L significantly<br />
improved <strong>the</strong> levels <str<strong>on</strong>g>of</str<strong>on</strong>g> GPx. It has been shown in earlier<br />
reports that vitamin C and E are capable <str<strong>on</strong>g>of</str<strong>on</strong>g> increasing <strong>the</strong><br />
renal GPx levels [4, 7, 46] and combinati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin C, E<br />
and lipoic acid ameliorated <strong>the</strong> testis GPx levels lowered<br />
due to lindane [42]. It is also c<strong>on</strong>cluded that <strong>the</strong> significant<br />
increase in <strong>the</strong> GPx levels was <strong>the</strong> maximum in case <str<strong>on</strong>g>of</str<strong>on</strong>g><br />
U?A?L group followed by U?L group and was least in<br />
A?L group.<br />
In <strong>the</strong> present study, <strong>the</strong> levels <str<strong>on</strong>g>of</str<strong>on</strong>g> GSH were decreased<br />
significantly in lindane treated group indicating <strong>the</strong> oxidative<br />
stress caused by lindane as also reported earlier [8, 22, 42, 48,<br />
67]. Decrease in renal GSH levels has also been documented<br />
in a case <str<strong>on</strong>g>of</str<strong>on</strong>g> alcohol [60], aflatoxin [61], gentamicin [1, 29],<br />
acetaminophen [27] and cisplatin [4] toxicity.<br />
The decrease in <strong>the</strong> GSH level as observed in <strong>the</strong> present<br />
study can be due to increased utilizati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> GSH for<br />
metabolism <str<strong>on</strong>g>of</str<strong>on</strong>g> lipid hydroperoxides by GPx or interacti<strong>on</strong><br />
<str<strong>on</strong>g>of</str<strong>on</strong>g> GSH with free radicals. Similar analogy is being also<br />
drawn in <strong>the</strong> earlier reports [5, 23].<br />
The levels <str<strong>on</strong>g>of</str<strong>on</strong>g> GSH were significantly ameliorated after<br />
<strong>the</strong> pretreatment with combinati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> antioxidants namely,<br />
vitamin C, E and a- lipoic acid (A?L group), <strong>cow</strong> <strong>urine</strong><br />
(U?L group) and combinati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> antioxidants and <strong>cow</strong><br />
<strong>urine</strong> (U?A?L group). Earlier studies have shown that<br />
vitamin C, E and lipoic acid attenuates <strong>the</strong> decreased renal<br />
GSH levels [4, 29]. Lindane induced decreased GSH levels<br />
were ameliorated by combinati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> lipoic acid, vitamin C,<br />
E and resveratrol [8] and lipoic acid, vitamin C and E [42]<br />
in brain and testis, respectively. The significant increase in<br />
GSH levels in <strong>the</strong> pretreatment groups was least in<br />
U?A?L group; intermediate in U?L group and maximum<br />
in A?L group.<br />
The present study reveals that lindane inhibits GPx and<br />
CAT due to its capacity to generate ROS, which will result<br />
in H 2 O 2 accumulati<strong>on</strong>. The increased H 2 O 2 in turn could<br />
cause SOD inhibiti<strong>on</strong> resulting in increased producti<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g><br />
superoxide radicals. Thus, increased producti<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> superoxide<br />
radicals would inhibit both CAT and GPx. Treatment<br />
with <strong>the</strong> adopted formulati<strong>on</strong> reduced <strong>the</strong> level <str<strong>on</strong>g>of</str<strong>on</strong>g> lipid<br />
peroxides indicating <strong>the</strong> effective antioxidant property <str<strong>on</strong>g>of</str<strong>on</strong>g><br />
<strong>the</strong> combinati<strong>on</strong> as well as <strong>cow</strong> <strong>urine</strong> al<strong>on</strong>e in <strong>the</strong> moderati<strong>on</strong><br />
<str<strong>on</strong>g>of</str<strong>on</strong>g> tissue damage.<br />
Antioxidant defense system protects <strong>the</strong> aerobic organism<br />
from <strong>the</strong> deleterious effects <str<strong>on</strong>g>of</str<strong>on</strong>g> reactive oxygen<br />
metabolites. Vitamin E, a major lipophilic antioxidant and<br />
vitamin C, play a vital role in <strong>the</strong> defense against oxidative<br />
stress [53]. In our study, <strong>the</strong> levels <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin E and C were<br />
decreased significantly during lindane intoxicati<strong>on</strong>. This is<br />
in agreement with <strong>the</strong> previous reports that oxidative stress<br />
results in deficiency in vitamin C and E [60, 61]. The<br />
increased oxidative stress due to lindane intoxicati<strong>on</strong> might<br />
have resulted in excess utilizati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin C and E,<br />
c<strong>on</strong>sequently, depleting <strong>the</strong>ir levels. The observed decrease<br />
in <strong>the</strong> level <str<strong>on</strong>g>of</str<strong>on</strong>g> kidney ascorbic acid and alpha tocopherol in<br />
lindane treated group could be as a result <str<strong>on</strong>g>of</str<strong>on</strong>g> increased<br />
utilizati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> <strong>the</strong>se antioxidants in scavenging <strong>the</strong> free<br />
radicals generated due to lindane.<br />
Moreover, it is well established that GSH in blood keeps<br />
up <strong>the</strong> cellular levels <str<strong>on</strong>g>of</str<strong>on</strong>g> <strong>the</strong> active forms <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin C and<br />
vitamin E by neutralizing <strong>the</strong> free radicals. When <strong>the</strong>re is a<br />
reducti<strong>on</strong> in <strong>the</strong> GSH <strong>the</strong> cellular levels <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin C is also<br />
lowered, indicating that GSH, vitamin C, and vitamin E are<br />
closely interlinked to each o<strong>the</strong>r [61]. In agreement with<br />
<strong>the</strong>se reports, <strong>the</strong> decreased levels <str<strong>on</strong>g>of</str<strong>on</strong>g> GSH, vitamin C and<br />
vitamin E <strong>on</strong> lindane administrati<strong>on</strong> were observed in our<br />
study.<br />
The pretreatment with combinati<strong>on</strong> <str<strong>on</strong>g>of</str<strong>on</strong>g> antioxidants in<br />
group A?L, with <strong>cow</strong> <strong>urine</strong> in group U?L and combinati<strong>on</strong><br />
<str<strong>on</strong>g>of</str<strong>on</strong>g> antioxidants and <strong>cow</strong> <strong>urine</strong> both in group U?A?L,<br />
resulted in significant increase in <strong>the</strong> endogenous levels <str<strong>on</strong>g>of</str<strong>on</strong>g><br />
vitamin C and E. The ameliorati<strong>on</strong> in <strong>the</strong> endogenous<br />
levels <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin C was <strong>the</strong> maximum in A?L group,<br />
followed by U?A?L group and minimum in U?L group.<br />
In c<strong>on</strong>trast, <strong>the</strong> significant increase in <strong>the</strong> levels <str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin<br />
E was <strong>the</strong> maximum in U?A?L group; intermediary in<br />
A?L group and least in U?L group. The increase in levels<br />
<str<strong>on</strong>g>of</str<strong>on</strong>g> vitamin C and E is obvious in <strong>the</strong> pretreatment groups<br />
A?L and U?A?L as <strong>the</strong>se were exogenously supplied<br />
with both vitamin C and E, however, <strong>the</strong> <strong>cow</strong> <strong>urine</strong> al<strong>on</strong>e<br />
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